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18 February 2025, Volume 29 Issue 5 Previous Issue   

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Stress distribution on the maxilla when wearing the Twin-block appliance for Class II malocclusion Li Shuai, Liu Hua, Shang Yonghui, Liu Yicong, Zhao Qihang, Liu Wen 2025, 29 (5):  881-887.  doi: 10.12307/2025.287 Abstract ( 250 )   PDF (1367KB) ( 204 )   Save BACKGROUND: The Twin-block orthodontic appliance is commonly used for the correction of Class II malocclusion. Its mechanism of action in stimulating mandibular growth has been confirmed in many studies, but its impact on maxillary growth is not very clear. OBJECTIVE: By establishing a finite element model to analyze the stress distribution of the maxillary complex, surrounding bone sutures, and maxillary dentition in patients with Class II malocclusion wearing Twin-block orthodontic appliances. METHODS: One patient with Class II malocclusion who underwent orthodontic treatment at Qingdao Hospital/Qingdao Municipal Hospital of Shandong Rehabilitation University was selected. The bite force data of the patient when wearing the Twin-block orthodontic appliance was measured, and CBCT data were collected. A finite element model was established, including the maxillary complex, peripheral sutures, Twin-block orthodontic appliance, and maxillary dentition. ABAQUS software was used to simulate the stress distribution in the maxilla and maxillary dentition when the patient was wearing the Twin-block appliance. RESULTS AND CONCLUSION: The equivalent stress on the maxillary anterior teeth was significantly smaller than that on the posterior teeth, and the maximum equivalent stress on both sides of the teeth were 4.797 5 MPa and 8.716 1 MPa, respectively, which were located at the first premolar. The maximum displacements were presented at the maxillary incisors on both sides of the teeth, which were 0.080 5 mm and 0.081 0 mm, respectively. The maximum equivalent stress on the bone suture was 1.284 MPa, which was mainly concentrated in the pterygopalatine suture and the frontal-maxillary suture on both sides, and there was almost no difference in the force of the rest of bone sutures; the maximum displacement of the bone suture was 0.07 mm, with the pterygopalatine suture having the largest displacement, followed by the frontal-maxillary suture. The maximal equivalent stress on the maxillary complex was 27.18 MPa, which was mainly concentrated on both sides of the anterior pyriform foramen of the maxilla, around the nasofrontal suture and around the pterygopalatine suture at the posterior part of the jaws. The maximal displacement of the maxilla was 0.07 mm, which was mainly concentrated on the maxillary alveolar bone. All these findings show that the occlusal force acts on the maxillary complex through the Twin-block appliance, resulting in clockwise rotation of the maxilla and steepening of the dentition plane. Measures should be taken to compensate for this tendency, for example, by considering maxillary molar elongation and intrusion in the process of occlusion, which are not only able to flatten the occlusal plane, but facilitate the mandibular protraction, thereby further improving Class II malocclusion orthodontic treatment.  Figures and Tables | References | Related Articles | Metrics

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Naringin inhibits iron deposition and cell apoptosis in bone tissue of osteoporotic rats  Lan Shuangli, Xiang Feifan, Deng Guanghui, Xiao Yukun, Yang Yunkang, Liang Jie 2025, 29 (5):  888-898.  doi: 10.12307/2024.593 Abstract ( 202 )   PDF (3763KB) ( 340 )   Save BACKGROUND: It has been found that abnormal apoptosis of bone tissue cells induced by abnormal iron metabolism plays an important role in the progression of osteoporosis. OBJECTIVE: To investigate the effect of naringin on iron metabolism and cell apoptosis in bone tissue of rats with osteoporosis.  METHODS: Fifty 2-month-old female Sprague-Dawley rats were randomly divided into five groups with 10 rats in each group: sham group, osteoporosis group, naringin low-dose group, naringin high-dose group, and naringin high-dose+DKK-1 group. Except for the sham group, rat models of osteoporosis were established by removing bilateral ovarian tissues in the other groups. At 8 weeks after modeling, rats in the naringin low- and high-dose groups were given 100 and 400 mg/kg/d naringenin by gavage, respectively, and rats in the naringenin high dose+DKK-1 group were given 400 mg/kg/d naringin  by gavage and subcutaneous injection of 25 mg/kg/d DKK-1, an inhibitor of the Wnt1 signaling pathway, for 7 consecutive days. Relevant indexes were detected after administration.  RESULTS AND CONCLUSION: Compared with the osteoporosis group, naringin could enhance the bone mineral density and serum calcium and superoxide dismutase levels in rats (P < 0.05), and reduce the serum levels of osteocalcin, malondialdehyde, and phosphorus (P < 0.05), while DKK-1 could partially inhibit the interventional effect of naringin (P < 0.05). Results from Micro-CT scanning, hematoxylin-eosin and TUNEL staining showed that compared with the osteoporosis group, naringin significantly improved bone microstructure and reduced the rate of cell apoptosis, while DKK-1 partially inhibited the interventional effect of naringin. Immunofluorescence staining results showed that compared with the osteoporosis group, naringin could reduce the oxygen content, anti-tartaric acid phosphatase expression, and elevate the expression of alkaline phosphatase in active tibia tissues (P < 0.05), while DKK-1 could partially inhibit the interventional effect of naringin (P < 0.05). Results from Prussian blue staining and immunohistochemical staining showed that compared with the osteoporosis group, naringin reduced iron deposition in bone and liver tissues as well as the expression of transferrin receptor 1 (P < 0.05), and elevated the protein expression of ferroportin 1 (P < 0.05) in bone tissue, and DKK-1 partially inhibited the intervention of naringin (P < 0.05). PCR and western blot assay of tibia specimens showed that compared with the osteoporosis group, naringin decreased the expression of anti-tartrate acid phosphatase, transferrin receptor 1 and Bax (P < 0.05), and elevated the expression of alkaline phosphatase, ferroportin 1, Bcl-2, Wnt1 and β-catenin (P < 0.05), while DKK-1 partially inhibited the interfering effect of naringin (P < 0.05). To conclude, naringin inhibits the progression of osteoporosis by reducing iron deposition and apoptosis rate in bone tissue, which may be related to the activation of the Wnt1 signaling pathway. Figures and Tables | References | Related Articles | Metrics

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MiR-338-3p affects proliferation and apoptosis of alveolar bone osteoblasts by targeting receptor activator of nuclear factor-kappaB ligand  Lang Mecuo, Zhang Yilin, Wang Li 2025, 29 (5):  899-907.  doi: 10.12307/2025.281 Abstract ( 169 )   PDF (2350KB) ( 75 )   Save BACKGROUND: MiR-338-3p could inhibit osteoclast differentiation, and downregulation of receptor activator of nuclear factor-κB ligand level could promote bone formation. However, it is unclear whether miR-338-3p can affect the proliferation and apoptosis of alveolar bone osteoblasts by regulating the receptor activator of nuclear factor-κB ligand level. OBJECTIVE: To explore the effect and mechanism of miR-338-3p on proliferation and apoptosis of alveolar bone osteoblasts by targeting receptor activator of nuclear factor-κB ligand.  METHODS: Human alveolar bone osteoblasts were isolated, transfected and treated with Wnt-C59 (Wnt/β-catenin pathway inhibitor), and divided into transfection control group, miR-338-3p group, miR-338-3p+control group, miR-338-3p+receptor activator of nuclear factor-κB ligand group and miR-338-3p+Wnt-C59 group. The dual luciferase report experiment was used to verify the regulatory effect of miR-338-3p on receptor activator of nuclear factor-κB ligand. Cell counting kit-8 and 5-Ethynyl-2’-deoxyuridine staining were used to detect cell proliferation levels. Flow cytometry was used to detect cell cycle and apoptosis levels. RT-qPCR was used to detect miR-338-3p, receptor activator of nuclear factor-κB ligand, Wnt-3a, β-Catenin, glycogen synthase kinase-3β mRNA levels. Western blot was used to detect RANKL, proliferating cell nuclear antigen, Ki67, CyclinD1, B-cell lymphoma/leukemia-2, B-cell lymphoma-2 related X protein, Caspase3, Wnt-3a, β-catenin, glycogen synthase kinase-3β protein levels.  RESULTS AND CONCLUSION: miR-338-3p could target the regulation of receptor activator of nuclear factor-κB ligand. After overexpression of miR-338-3p, cell survival rate, 5-Ethynyl-2’-deoxyuridine positive cell rate, proportion of S-phase cells were increased, and apoptosis rate was decreased. The mRNA and protein levels of miR-338-3p, proliferating cell nuclear antigen, Ki67, CyclinD1, B-cell lymphoma/leukemia-2, Wnt-3a, and β-catenin were increased, while the mRNA and protein levels of B-cell lymphoma-2 related X protein, Caspase3 protein, receptor activator of nuclear factor-κB ligand, and glycogen synthase kinase-3β were decreased (all P < 0.05). Overexpression of receptor activator of nuclear factor-κB ligand or Wnt-C59 could weaken the effects of overexpression of miR-338-3p on cell proliferation and apoptosis (all P < 0.05). Overall, miR-338-3p promotes alveolar bone osteoblast proliferation and inhibits apoptosis by targeting receptor activator of nuclear factor-κB ligand, which may act through activation of the Wnt/β-catenin signaling pathway. Figures and Tables | References | Related Articles | Metrics

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Resveratrol activates extracellular-regulated protein kinase 5 signaling protein to promote proliferation of mouse MC3T3-E1 cells  Niu Yongkang, Feng Zhiwei, Wang Yaobin, Liu Zhongcheng, Xiang Dejian, Liang Xiaoyuan, Yi Zhi, Zhan Hongwei, Geng Bin, Xia Yayi 2025, 29 (5):  908-916.  doi: 10.12307/2025.209 Abstract ( 192 )   PDF (2492KB) ( 461 )   Save BACKGROUND: The extracellular-regulated protein kinase 5 (ERK5) signaling protein is essential for the survival of organisms, and resveratrol can promote osteoblast proliferation through various pathways. However, whether resveratrol can regulate osteoblast function through the ERK5 signaling protein needs further verification. OBJECTIVE: To explore the regulatory effect of ERK5 on the proliferation of MC3T3-E1 cells and related secreted proteins, and to further verify whether resveratrol can complete the above process by activating ERK5. METHODS: Mouse MC3T3-E1 preosteoblasts were treated with complete culture medium, XMD8-92 (an ERK5 inhibitor), epidermal growth factor (an ERK5 activator), resveratrol alone, XMD8-92+EGF, and resveratrol+XMD8-92, respectively. Western blot assay was used to detect the expression of ERK5 and p-ERK5 proteins, proliferation-related proteins Cyclin D1, CDK4 and PCNA, and osteoblast-secreted proteins osteoprotegerin and receptor activator of nuclear factor-κB ligand in MC3T3-E1 cells of each group. The fluorescence intensity of ERK5, osteoprotegerin and receptor activator of nuclear factor-κB ligand in each group was detected by cell immunofluorescence staining, and cell proliferation was detected by EdU staining, respectively. The appropriate concentration and time of resveratrol intervention in MC3T3-E1 cells were determined by cell morphology observation and cell counting kit-8 assay. RESULTS AND CONCLUSION: The activation of ERK5 signaling protein could effectively promote the proliferation of MC3T3-E1 cells, up-regulate the osteoprotegerin/receptor activator of nuclear factor-κB ligand ratio. The appropriate concentration and time for resveratrol intervention in MC3T3-E1 cells was 5 μmol/L and 24 hours, respectively. Resveratrol could activate ERK5 signaling protein, thereby promoting osteoblast proliferation and up-regulating the osteoprotegerin/RANKL ratio. All these results indicate that resveratrol can promote the proliferation of MC3T3-E1 cells and up-regulate the osteoprotegerin/RANKL ratio by activating the ERK5 signaling protein. Figures and Tables | Related Articles | Metrics

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Therapeutic effect and mechanism by which Trichosanthis Fructus-Allii Macrostemonis Bulbus regulates gut microbiota in a rat model of coronary heart disease #br# #br# Sun Guanghan, Xie Zhencong, Sun Mi, Xu Yang, Guo Dong 2025, 29 (5):  917-927.  doi: 10.12307/2025.236 Abstract ( 210 )   PDF (6254KB) ( 185 )   Save BACKGROUND: A network-based pharmacological approach has identified multifunctional effects of the main bioactive compounds in the Trichosanthis Fructus-Allii Macrostemonis Bulbus on coronary heart disease; however, the mechanism of its therapeutic effect on coronary heart disease has not been fully elucidated. OBJECTIVE: To investigate the role and mechanism of Trichosanthis Fructus-Allii Macrostemonis Bulbus in improving coronary heart disease by regulating the composition of gut microbiota. METHODS: Forty Sprague-Dawley rats were randomly divided into four groups: blank control group (n=10), model group (n=10), positive drug group (n=10), and medicine pair group (n=10). A rat model of coronary heart disease was established by continuous gastric perfusion of fat emulsion and injection of pituitrin. After modeling, rats in the model group were gavaged with distilled water (10 mL/kg) for control, rats in the positive drug group were gavaged with simvastatin 4 mg/kg per day, and rats in the medicine pair group were gavaged with Trichosanthis Fructus-Allii Macrostemonis Bulbus pairs 7.56 g/kg per day. All interventions lasted for 14 days. Electrocardiograms and myocardial pathology were observed, and blood lipid levels were measured. The structure of gut microbiota was analyzed using 16S rDNA sequencing technology. RESULTS AND CONCLUSION: Electrocardiogram results showed ST segment elevation in the model group. There were no significant abnormalities in the electrocardiograms of the positive drug group and medicine pair group. Compared with the blank control group, the levels of total cholesterol, triacylglycerol, and low-density lipoprotein cholesterol were significantly higher in the model group (P < 0.05). Compared with the model group, the levels of total cholesterol, triacylglycerol, and low-density lipoprotein cholesterol were significantly lower in the positive drug group and medicine pair group (P < 0.05). Compared with the blank control group, focal myocardial cell necrosis was observed in the model group, while partial myocardial cell disarray was observed in the positive drug group and medicine pair group. Compared with the blank control group, the Ace, Shannon, and Chao indices were increased (P < 0.05) and the Simpson index was decreased (P < 0.05) in the model group, positive drug group and medicine pair group. Compared with the model group, the Ace and Chao indices were decreased (P < 0.05), while the Shannon index showed no significant difference (P > 0.05) and the Simpson index was also decreased (P < 0.05) in the positive drug group and medicine pair group. Compared with the blank control group, the relative abundances of Desulfovibrionia, Muribaculaceae_norank, etc. were increased in the model group, while those of Clostridia, [Eubacterium]_coprostanoligenes_group_norank, etc. were decreased. Compared with the model group, the relative abundances of WPS-2_norank, Muribaculaceae_norank, etc. were increased in the medicine pair group, while those of Clostridia, [Eubacterium]_coprostanoligenes_group_norank, etc. were decreased; the relative abundances of Desulfobacterota, [Eubacterium]_coprostanoligenes_group_norank, etc. were increased in the positive drug group, while those of Firmicutes, Muribaculaceae_norank, etc. were decreased. Compared with the positive drug group, the relative abundances of Desulfobacterota, Bacteroides, etc. were increased in the medicine pair group, while those of Firmicutes, [Eubacterium]_coprostanoligenes_group_norank, etc. were decreased. The LEfSe results showed that the medicine pair group had the highest microbial enrichment, followed by the blank control group and positive drug group, with the model group having the lowest microbial enrichment. To conclude, Trichosanthis Fructus-Allii Macrostemonis Bulbus pairs can improve the development of coronary heart disease by regulating gut microbiota composition, providing new insights for further research and development of Trichosanthis Fructus-Allii Macrostemonis Bulbus pairs. Figures and Tables | References | Related Articles | Metrics

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Effect of lncRNA-TNFRSF13C on hypoxia-inducible factor 1alpha in periodontal cells by modulation of #br# miR-1246 #br# Bai Jing, Zhang Xue, Ren Yan, Li Yuehui, Tian Xiaoyu 2025, 29 (5):  928-935.  doi: 10.12307/2025.296 Abstract ( 214 )   PDF (1313KB) ( 91 )   Save BACKGROUND: LncRNA-TNFRSF13C, an important factor in B cell development and function, is expressed in periodontal tissues of patients with periodontitis, but the specific mechanism is still unclear. OBJECTIVE: To investigate the mechanism of lncRNA-TNFRSF13C regulating miR-1246 on hypoxia-inducible factor 1α in periodontal cells.  METHODS: Human periodontal ligament cells (hPDLCs) were treated with lipopolysaccharide and divided into group A (hPDLCs cell lines without transfection), group B (hPDLCs cell lines transfected with TNFRSF13C NC-siRNA), group C (hPDLCs cell lines transfected with TNFRSF13C-siRNA), group D (hPDLCs cell line transfected with miR-1246 mimics), group E (hPDLCs cell line transfected with miR-1246 siRNA), group F (hPDLCs cell line transfected with TNFRSF13C-siRNA+miR-1246 mimics), and group G (hPDLCs cell line transfected with TNFRSF13C-siRNA+miR-1246 siRNA). The relative expression of lncRNA-TNFRSF13C and miR-1246 in each group was detected by qRT-PCR. Cell counting kit-8 assay was used to detect cell viability. Apoptosis was detected by flow cytometry. Expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins was detected by western blot. The correlation between lncRNA-TNFRSF13C and miR-1246 was analyzed by Pearson, and the targeting relationship was analyzed by dual-luciferase reporter assay. RESULTS AND CONCLUSION: There was no significant difference in human periodontal ligament cell activity, apoptosis rate and protein indexes between groups A and B (P >0.05). Compared with group B, hPDLCS cell activity in group C was increased, and apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins were decreased (P < 0.05). Compared with group C, hPDLCS cell activity in group D was decreased, and apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins were increased (P < 0.05). Compared with group D, the cell activity of group E was increased (P < 0.05). The cell activity in group F was lower than that in group E, and the apoptosis rate was reduced in both groups E and F (P < 0.05). Compared with group F, the cell activity of group G was increased, and the apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor were decreased (P < 0.05). LncRNA-TNFRSF13C was positively correlated with miR-1246 (P < 0.05). Compared with the TNFRSF13C-siRNA group, the fluorescence activity of miR-1246-wt in the TNFRSF13C-NC group was reduced (P > 0.05); compared with the miR-1246-NC group, the fluorescence activities of hypoxia-inducible factor 1α-wt and vascular endothelial growth factor-wt in the miR-1246 mimics group were increased (P < 0.05). To conclude, down-regulation of lncRNA-TNFRSF13C can promote the activity of periodontal cells treated with lipopolysaccharide, reduce apoptosis, and inhibit hypoxia-inducible factor 1α and vascular endothelial growth factor. The mechanism is related to the regulation of miR-1246 activity. Figures and Tables | References | Related Articles | Metrics

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Analgesic effect of acupuncture in a rat model of lumbar disc herniation  Zhi Fang, Zhu Manhua, Xiong Wei, Lin Xingzhen 2025, 29 (5):  936-941.  doi: 10.12307/2025.250 Abstract ( 228 )   PDF (1105KB) ( 162 )   Save BACKGROUND: Acupuncture is an effective method for lumbar pain in lumbar disc herniation, but its mechanism has not yet been clarified. Factors related to the JAK2/STAT3 signaling pathway regulate the body’s inflammatory response and are involved in the process of neuropathic pain. OBJECTIVE: To study the mechanism of acupuncture on lumbar disc herniation in a rat model based on the JAK2/STAT3 signaling pathway.  METHODS: Forty Sprague-Dawley rats were randomly divided into four groups: sham operation group, model group, acupuncture group, and acupuncture+agonist group, with 10 rats in each group. Animal models of L5 lumbar disc herniation was constructed through autologous disc cell transplantation in the model group, acupuncture group, and acupuncture+agonist group. Rats in the acupuncture group and the acupuncture+agonist group received acupuncture treatment (Yanglingquan, Shenshu, Huantiao, and Dachangshu acupoints) at 3 days after modeling, and acupuncture treatment was given once a day, 20 minutes each, for 15 consecutive days. Rats in the acupuncture+agonist group were injected intrathecally with coumermycin A1, a JAK2 agonist, into the L4/L5 intervertebral space, once a day, 20 minutes each, prior to the acupuncture at 6, 12, and 18 days after modeling. Paw withdrawal mechanical threshold was detected before and 3, 6, 9, 12, 15, and 18 days after modeling. At 18 days after modeling, serum inflammatory factor levels were detected, hematoxylin-eosin staining was performed to observe the morphology of L5-L6 tissues, RT-PCR was performed to detect the expression of JAK2 and STAT3 mRNAs in L5-L6 tissues, and western blot was performed to detect the expression of JAK2, p-JAK2 and p-STAT3 proteins in L5-L6 tissues.  RESULTS AND CONCLUSION: The paw withdrawal mechanical thresholds of rats in the model group at different time points after modeling were lower than those in the sham operation group (P < 0.05), the paw withdrawal mechanical thresholds of rats in the acupuncture group were higher than those in the model group at 9, 12, 15, and 18 days after modeling (P < 0.05), and the paw withdrawal mechanical thresholds of rats in the acupuncture+agonist group were lower than those in the acupuncture group at 9, 12, 15, and 18 days after modeling (P < 0.05). The levels of interleukin 6, tumor necrosis factor α, neurotransmitter substance P, and brain neuropeptide Y were elevated in the model group compared with the sham operation group (P < 0.05); the levels of all four inflammatory factors were reduced in the acupuncture group compared with the model group (P < 0.05); and the levels of all four inflammatory factors were elevated in the acupuncture+agonist group compared with the acupuncture group (P < 0.05). Hematoxylin-eosin staining showed that lumbar degeneration was obvious in the model group but reduced in the acupuncture group and the acupuncture+agonist group. Moreover, the reduction was more obvious in the acupuncture group compared with the acupuncture+agonist group. The JAK2 and STAT3 mRNA expression as well as the p-JAK2 and p-STAT3 protein expression were elevated in the model group compared with the sham operation group (P < 0.05), were decreased in the acupuncture group compared with the model group (P < 0.05), and were increased in the acupuncture+agonist group compared with the acupuncture group (P < 0.05). To conclude, acupuncture can alleviate inflammation to exert analgesic effects in the rat model of lumbar disc herniation, and its mechanism of action may be related to the inhibition of the JAK2/STAT3 signaling pathway. Figures and Tables | References | Related Articles | Metrics

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Effect of pravastatin on functional recovery from sciatic nerve crush injury in rats  Liu Zan, An Ran, Li Baocheng 2025, 29 (5):  942-950.  doi: 10.12307/2025.248 Abstract ( 260 )   PDF (1401KB) ( 192 )   Save BACKGROUND: Pravastatin is a clinically effective drug for the treatment of hypercholesterolemia and is now found to play a beneficial role in the treatment of CNS injury; however, the mechanism remains unknown. OBJECTIVE: To ascertain the possible mechanism of action and whether pravastatin medication can expedite functional recovery following sciatic nerve crush injury. METHODS: Male Sprague-Dawley rats were randomly assigned into: pravastatin (sciatic nerve crush injury+pravastatin gavage), negative control (sciatic nerve crush injury+saline gavage), and sham operation (sciatic nerve exposure but no injury+saline gavage). While the other two groups received comparable amounts of saline gavage, the pravastatin group received postoperative pravastatin (5 mg/kg) by gavage for 1 week. The general conditions of the rats in each group were observed after operation. Sciatic function index was evaluated at the end of the 2nd, 4th, 6th, and 8th week after operation, and the wet mass ratio of the gastrocnemius muscle was measured at the end of the 8th week after operation. The levels of inflammatory cytokines in serum were measured using ELISA. Histomorphometrics was used to measure the number of myelinated nerve fibers, fiber diameter, axon diameter, and myelin sheath thickness. RT-qPCR assay was used to measure the relative mRNA expression of nerve growth factor and brain-derived neurotrophic factor, and western blot was used to measure the protein expression of growth-associated protein 43. RESULTS AND CONCLUSION: Compared with the negative control group, the sciatic function index in the pravastatin group recovered faster (P < 0.05) and was closer to the level of the sham operation group, the expression of tumor necrosis factor α and interleukin 6 in serum was lower (P < 0.05) and close to that of the sham operation group, and the relative mRNA expression of nerve growth factor and brain-derived neurotrophic factor in the sciatic nerve increased (P <  0.05 or P < 0.01), the relative protein expression of growth-associated protein 43 in the sciatic nerve was also significantly increased (P < 0.05), the number of myelinated nerve fibers was increased more, and the values of fiber diameter, axon diameter, and myelin sheath thickness were larger (P < 0.01) and closer to those of the sham operation group. To conclude, treatment with pravastatin accelerates functional recovery from sciatic nerve crush injury by a possible mechanism of inhibiting the expression of tumor necrosis factor α and interleukin 6 and promoting the secretion of neurotrophic factors nerve growth factor and brain-derived neurotrophic factor. Figures and Tables | References | Related Articles | Metrics

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Compressive stress induces degeneration of cartilaginous endplate cells through the SOST/Wnt/beta-catenin pathway Xiang Pan, Che Yanjun, Luo Zongping 2025, 29 (5):  951-957.  doi: 10.12307/2025.277 Abstract ( 243 )   PDF (1207KB) ( 126 )   Save BACKGROUND: Many factors can cause disc degeneration, including aging, nutritional deficiency, and mechanical factors. The mechanical load is considered to be a very important factor, but its mechanism is still unclear.OBJECTIVE: To investigate the role of sclerostin (SOST) and Wnt/β-catenin signaling pathways in inducing degeneration of endplate cartilage.  METHODS: Cartilage endplate cells were extracted from 4-week-old male Sprague-Dawley rats. Compressive stress was applied to endplate chondrocytes in vitro using a mechanical loading apparatus, and the cell viability was determined by the cell counting kit-8 assay at 1, 3, 5, and 7 days after compression. Western blot, reverse transcription quantitative PCR, and cellular immunofluorescence techniques were employed to examine intracellular cartilage markers (Aggrecan and type II collagen) as well as calcification-related factors (Runx2 and osteocalcin). The expression of extracellular matrix degradation enzyme and genes related to the signaling pathway (SOST and β-catenin) was also analyzed.  RESULTS AND CONCLUSION: Under compressive stress, the cell activity of endplate chondrocytes increased with both the duration and intensity of stress. Furthermore, the expression levels of Aggrecan and type II collagen decreased in endplate cells under compressive stress, while those of calcification-related factors (Runx2 and osteocalcin) increased. Additionally, compressive stress promoted extracellular matrix degradation in endplate chondrocytes, leading to an increase in matrix metalloproteinase 3 and matrix metalloproteinase 13 expression. Abnormalities were observed in the Wnt/β-catenin signaling pathway within these cells under compressive stress, characterized by a decrease in specific inhibitory factor SOST expression accompanied by abnormal accumulation of β-catenin. To conclude, decreased SOST expression in endplate chondrocytes under compressive stress activates the Wnt/β-catenin signaling pathway, thereby promoting calcification, degeneration and extracellular matrix degradation in the cartilage endplate. Figures and Tables | References | Related Articles | Metrics

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Prostaglandin E1 regulates vascular-related factors and protects microcirculatory function during the acute phase of traumatic spinal cord injury  Wang Rongrong, Huang Yushan, Li Xiangmiao, Bai Jinzhu 2025, 29 (5):  958-967.  doi: 10.12307/2025.203 Abstract ( 224 )   PDF (1342KB) ( 124 )   Save BACKGROUND: Prostaglandin E1 (PGE1) has been shown to play a regulatory role in vasodilatation, inflammation, and leukocyte migration and adhesion, but its effects on spinal cord microcirculation after traumatic spinal cord injury (SCI) remain poorly understood. OBJECTIVE: To investigate the mechanism underlying the protective effects of PGE1 administered during the acute phase of traumatic SCI in rats on the regulation of vascular-related factors and microcirculatory function. METHODS: Seventy-two female Sprague-Dawley rats were divided into three groups (n=24 per group): control group, SCI group, and PGE1 group. An in vivo SCI model was established using Allen’s blow method. Rats in the PGE1 group were injected with PGE1 (10 µg/kg) via the tail vein immediately after SCI. Spinal cord microcirculatory blood flow and oxygen saturation, spinal cord microvessel diameter and area, spinal cord water content, vascular function regulators (von Willebrand factor, thromboxane A2, prostacyclin, endothelin-1), and inflammatory factors (tumor necrosis factor-α, interleukin-1β) were measured at 2 and 24 hours after SCI. RESULTS AND CONCLUSION: At 2 hours after SCI, the diameter and area of spinal cord microvessels, spinal cord microcirculatory blood flow, and oxygen saturation in the PGE1 group were higher than those in the SCI group (P < 0.05), the water content of the spinal cord was lower than that in the SCI group  (P < 0.05), and the level of plasma von Willebrand Factor, the ratio of thromboxane A2/prostacyclin of the spinal cord and the level of endothelin-1 were lower than those in the SCI group (P < 0.05). At 24 hours after SCI, the spinal cord microvessel area, blood flow, and oxygen saturation of rats in the PGE1 group were higher than those in the SCI group (P < 0.05), the spinal cord water content was lower than that in the SCI group (P < 0.05), and the levels of plasma von Willebrand factor, spinal cord tissue thromboxane A2/prostacyclin ratio and the levels of endothelin-1, tumor necrosis factor-α and interleukin-1β were lower than those in the SCI group (P < 0.05). The diameter and area of spinal cord microvessels, spinal cord microcirculatory blood flow and blood oxygen saturation of rats in the SCI group were higher than those in the SCI group at 24 hours post-injury (P < 0.05), and the levels of plasma von Willebrand factor, spinal tissue thromboxane A2/prostacyclin ratio, tumor necrosis factor-α and interleukin-1β were higher than those at 2 hours post-injury (P < 0.05), but the level of endothelin-1 in spinal cord tissue was lower than that at 2 hours (P < 0.05). The blood flow and oxygen saturation of spinal cord microcirculation in the PGE1 group rats at 24 hours post-injury were lower than those at 2 hours post-injury (P < 0.05), and the diameter and area of spinal cord microvessels and water content of the spinal cord were higher than those at 2 hours post-injury (P < 0.05). The above results indicate that intravenous administration of PGE1 in SCI rats immediately after injury can regulate vascular function regulators, inflammatory factors and improve microcirculation of the spinal cord after SCI, which provides a potential basis for the search of drugs for the treatment of acute SCI. Figures and Tables | References | Related Articles | Metrics

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Effect of fibroblast growth factor receptor 1 inhibitor on bone destruction in rats with collagen-induced arthritis  Han Haihui, Meng Xiaohu, Xu Bo, Ran Le, Shi Qi, Xiao Lianbo 2025, 29 (5):  968-977.  doi: 10.12307/2025.293 Abstract ( 210 )   PDF (2531KB) ( 135 )   Save BACKGROUND: Preliminary research by our group suggests that targeting fibroblast growth factor receptor 1 (FGFR1) may be an effective strategy for treating RA. OBJECTIVE: To investigate the effects of an FGFR1 inhibitor (PD173074) on bone destruction in rats with collagen-induced arthritis.  METHODS: Twenty-five female Sprague-Dawley rats were randomly divided into five groups: normal control group, model group, methotrexate group, low-dose PD173074 group, and high-dose PD173074 group. Except for the normal control group, rat models of type II collagen-induced arthritis were made in each group. After successful modeling, rats were injected intraperitoneally with sterile PBS in the normal and model groups, 1.04 mg/kg methotrexate in the methotrexate group, and 5 and 20 mg/kg in the low-dose group and high-dose PD173074 groups, once a week. After 4 weeks of drug administration, clinical symptoms and joint swelling in rats were observed. Micro-CT was used for three-dimensional reconstruction and analysis of the ankle joints. Pathological changes in the ankle joints were observed. Periarticular angiogenesis and the expression of receptor activator of nuclear factor-κB ligand were detected. The expression levels of p-FGFR1, vascular endothelial growth factor A, and tartrate-resistant acid phosphatase in the synovial membrane were measured. Pathological changes in the liver, spleen, and kidney were observed and liver, spleen, and kidney indices were calculated.  RESULTS AND CONCLUSION: PD173074 could alleviate clinical symptoms and joint swelling, delay bone loss, improve bone structure, reduce synovial invasion and cartilage bone erosion, reduce the number of periarticular osteoclasts, inhibit angiogenesis in synovial tissues, reduce the expression of receptor activator of nuclear factor-κB ligand, and inhibit the expression of FGFR1 phosphorylated protein, tartrate-resistant acid phosphatase and vascular endothelial growth factor A. Pathologic observation of the liver, spleen and kidney in rats showed no obvious toxic side effects after PD173074 treatment. To conclude, the FGFR1 inhibitor can delay the progression of joint inflammation and bone destruction and inhibit angiogenesis in the rat model of type II collagen-induced arthritis. The therapeutic effect of PD173074 has been preliminarily validated in the type II collagen-induced arthritis model and may act by inhibiting FGFR1 phosphorylation, which provides a direction for the search of new therapeutic targets for rheumatoid arthritis.    Figures and Tables | References | Related Articles | Metrics

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Mechanism of immunosuppression in rats by herb-partitioned moxibustion based on transcriptome sequencing technology Tian Yuefeng, Xiong Luojie, Wang Huifang, Zhai Chuntao, Li Wei 2025, 29 (5):  978-988.  doi: 10.12307/2025.276 Abstract ( 206 )   PDF (4211KB) ( 335 )   Save BACKGROUND: Immunosuppression leads to impaired body immune function and aggravates the disease. Herb-partitioned moxibustion can effectively regulate immune function and improve immunity in the body, but its regulatory mechanism has not been elucidated. OBJECTIVE: To sequence immunosuppressed model rats treated with herb-partitioned moxibustion using bioinformatics techniques based on transcriptomics and to explore the mechanisms by which it regulates immunity.  METHODS: Twenty-four Sprague-Dawley rats were randomly assigned to three groups: control, model, and herb-partitioned moxibustion groups, with eight rats in each group. The model and herb-partitioned moxibustion groups were subjected to establishment of an immune suppression model by intraperitoneal injection of cyclophosphamide at a dose of 35 mg/kg for 3 consecutive days. No interventions were administered to the control and model groups after modeling. In contrast, the herb-partitioned moxibustion group received moxibustion treatment at Zhongwan, Shenque, Guanyuan, and Zusanli acupoints using a combination of moxa and herbal cakes, once a day, for 10 consecutive days, with samples being collected the day after the end of the intervention. Peripheral blood was collected from all groups of rats to measure their white blood cell count. RNA-seq was performed on the Illumina sequencing platform, and differentially expressed genes were selected for bioinformatics analysis using the GO and KEGG databases.  RESULTS AND CONCLUSION: Compared with the control group, the model group exhibited a significant decrease in white blood cell count (P < 0.001). RNA-seq analysis identified 3 026 differentially expressed genes between the model and control groups, with 1 565 upregulated and 1 461 downregulated. There were 535 differentially expressed genes identified between the herb-partitioned moxibustion group and the model group, with 280 upregulated and 255 downregulated. The Venn diagram analysis revealed that 159 genes were downregulated in the model group compared with the control group. However, after moxibustion with herbal cakes, these genes were upregulated. Protein-protein interaction network analysis identified 10 core targets, including Oasl, Oas2, Isg15, Herc6, Mx2, Helz2, Mx1, Syk, Hspa1a, and Ret. According to GO and KEGG analyses, moxibustion with herbal cakes regulated the body through pathways related to immune response, viruses, angiogenesis, and the autoimmune system. To conclude, there is a significant association between herbal cake-separated moxibustion intervention and immune suppression targets, including Oasl, Oas2, Isg15, Herc6, Mx2, Helz2, and Mx1. The intervention exhibits regulatory effects in the pathways related to immune responses, viral activities, and angiogenesis. Figures and Tables | References | Related Articles | Metrics

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Dimethyl fumarate alleviates nerve damage in a mouse model of Parkinson’s disease  Lu Ranran, Zhou Xu, Zhang Lijie, Yang Xinling 2025, 29 (5):  989-994.  doi: 10.12307/2025.294 Abstract ( 222 )   PDF (1152KB) ( 124 )   Save BACKGROUND: Parkinson’s disease is a multifactorial neurological disorder characterized by progressive loss of dopaminergic neurons, and dimethyl fumarate (DMF) has potent neuroprotective and immunomodulatory effects in neurodegenerative diseases. OBJECTIVE: To explore the neuroprotective mechanism of DMF in a mouse model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson’s disease. METHODS: Twenty-four C57BL/6 mice were selected and randomly divided into control group, model group, low-dose DMF, and high-dose DMF groups. An animal model of Parkinson’s disease was established in the latter three groups by intraperitoneal injection of 30 mg/kg MPTP, once a day for 5 consecutive days. Intragastric administration was given 30 minutes after each injection of MPTP. Mice in the low-dose DMF group (30 mg/kg) and high-dose DMF group  (50 mg/kg) were intragastrically administered once a day for 7 consecutive days. The control and model groups were initially administered the same dose of normal saline. Behavioral testing, western blot, oxidative stress marker detection, and immunohistochemical staining were used to analyze the regulatory effects of DMF on oxidative stress and Keap1/Nrf2 signaling pathway in MPTP-induced Parkinson’s disease mice, as well as the protective mechanism of DMF on degeneration of dopamine neurons. RESULTS AND CONCLUSION: Compared with the model group, mice in the low-dose DMF group exhibited significant improvements in motor retardation and postural imbalance (P < 0.01), with even more remarkable improvements observed in the high-dose DMF group (P < 0.01). Compared with the control group, the model group showed a significant increase in the oxidative stress marker malondialdehyde and a decrease in superoxide dismutase expression  (P < 0.01). Compared with the model group, the low-dose DMF group reduced malondialdehyde production and increased superoxide dismutase expression (P < 0.01), and similar improvements were observed in the high-dose DMF group (P < 0.01). Immunohistochemical and western blot assays demonstrated a significant decrease in the number of dopaminergic neurons and tyrosine hydroxylase protein expression in the substantia nigra of mice in the model group compared with the control group (P < 0.01). However, in the low-dose DMF group, there was an increase in the number of dopaminergic neurons and tyrosine hydroxylase protein expression in the substantia nigra (P < 0.01), with even more significant improvements in the high-dose DMF group (P < 0.01). Western blot results revealed that the model group exhibited elevated Keap1 protein expression and decreased Nrf2 protein expression. In contrast, the DMF groups showed reduced Keap1 protein expression and increased Nrf2 protein expression compared to the model group (P < 0.01). To conclude, DMF regulates the Keap1/Nrf2 pathway in the substantia nigra of mice with Parkinson’s disease, and this regulatory effect is positively correlated with the dose of DMF (P < 0.01). Therefore, we infer that DMF exerts neuroprotective effects through the Keap1/Nrf2 signaling pathway. Figures and Tables | References | Related Articles | Metrics

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Constructing rabbit intervertebral disc degeneration models by different methods under X-ray guidance: a comparative study  Ding Zhili, Huang Jie, Jiang Qiang, Li Tusheng, Liu Jiang, Ding Yu 2025, 29 (5):  995-1002.  doi: 10.12307/2025.249 Abstract ( 205 )   PDF (2991KB) ( 115 )   Save BACKGROUND: Scholars at home and abroad consider New Zealand rabbits to be an ideal model animal because of the similar anatomical morphology of the lumbar spine to that of the human lumbar spine. There is a lack of systematic comparison of different ways to establish rabbit intervertebral disc degeneration models under X-ray guidance. OBJECTIVE: To establish a rabbit model of lumbar disc degeneration using X-ray guided acupuncture, end-plate injection and combined method, and to compare the modeling effects of these three methods. METHODS: Eighteen 6-month-old New Zealand white rabbits were randomly selected and divided into four groups: acupuncture group, endplate injection group, combined group and blank control group. In the acupuncture group, three consecutive segments of the intervertebral discs (L2/3, L3/4, L4/5) were needled and modeled; in the endplate injection group, 50 μL of anhydrous ethanol was injected at a single point on the endplates of the three consecutive segmental discs; in the combined group, three consecutive segmental intervertebral discs were needled and injected with 50 μL of anhydrous ethanol at four azimuthal points on the endplates of the corresponding segmental discs; and the blank control group received no interventions. X-ray examination was performed to measure the disc height index at 2, 4, and 8 weeks after surgery. The intervertebral disc tissues were then taken for anatomical observation and pathological examination.  RESULTS AND CONCLUSION: (1) Anatomical examination showed that fibrous annulus rupture, nucleus pulposus degeneration, and total disc structure disorder were the main manifestation in the acupuncture group, endplate injection group, and combined group, respectively. (2) X-ray examination showed that the disc height index showed the most obvious reduction in the acupuncture group at 2 weeks after operation, significant reductions in the endplate injection group at 2 and 4 weeks after operation, and significant reductions in the combined group at 2, 4, and 8 weeks after operation. (3) Pathological examination showed that the fibrous ring structure was damaged and the inner annulus fibrosus protruded inward in the acupuncture group; endplate fissure, disordered arrangement and nucleus loss were observed in the endplate injection group; total disc structure disorder with the nucleus pulposus losing water and shrinking and no obvious border with the broken annulus fibrosus was found in the combined group. To conclude, acupuncture, endplate injection and the modified endplate injection method can establish the rabbit intervertebral disc degeneration model. Compared with the single method, the modified endplate injection method can greatly accelerate and aggravate the degeneration of the intervertebral disc, and can effectively shorten the experiment period. Figures and Tables | References | Related Articles | Metrics

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Metformin exerts a protective effect on articular cartilage in osteoarthritis rats by inhibiting the PI3K/AKT/mTOR pathway  Xu Tianjie, Fan Jiaxin, Guo Xiaoling, Jia Xiang, Zhao Xingwang, Liu kainan, Wang Qian 2025, 29 (5):  1003-1012.  doi: 10.12307/2025.282 Abstract ( 278 )   PDF (3399KB) ( 143 )   Save BACKGROUND: Studies have shown that metformin has anti-inflammatory, anti-tumor, anti-aging and vasoprotective effects, and can inhibit the progression of osteoarthritis, but its specific mechanism of action remains unclear. OBJECTIVE: To investigate the mechanism of metformin on cartilage protection in a rat model of osteoarthritis. METHODS: Forty male Sprague-Dawley rats were randomly divided into four groups (n=10 per group): blank, control, sham-operated, and metformin groups. The blank group did not undergo any surgery. In the sham-operated group, the joint cavity was exposed. In the model group and the metformin group, the modified Hulth method was used to establish the osteoarthritis model. At 1 day after modeling, the rats in the metformin group were given 200 mg/kg/d  metformin by gavage, and the model, blank, and sham-operated groups were given normal saline by gavage. Administration in each group was given for 4 weeks consecutively. Hematoxylin-eosin staining, toluidine blue staining, and safranin O-fast green staining were used to observe the morphological structure of rat knee joints. Immunohistochemical staining and western blot were used to detect the protein expression of SOX9, type II collagen, a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5), Beclin1, P62, phosphatidylinositol 3-kinase (PI3K), p-PI3K, protein kinase B (AKT), p-AKT, mammalian target of rapamycin (mTOR), and p-mTOR in rat cartilage tissue. RESULTS AND CONCLUSION: The results of hematoxylin-eosin, toluidine blue and safranin O-fast green staining showed smooth cartilage surface of the knee joints and normal histomorphology in the blank group and the sham-operated group, while in the model group, there was irregular cartilage surface of the knee joint and cartilage damage, with a decrease in the number of chondrocytes and the content of proteoglycans in the cartilage matrix. In the metformin group, there was a significant improvement in the damage to the structure of the cartilage in the knee joints of the rats, and the cartilage surface tended to be smooth, with an increase in the number of chondrocytes and the content of proteoglycans in the cartilage matrix. Immunohistochemistry staining and western blot results showed that compared with the control and sham-operated groups, the expression of SOX9, type II collagen, and Beclin1 proteins in the cartilage tissue of rats in the model group was significantly decreased (P < 0.05). Conversely, the expression of ADAMTS5, P62, as well as p-PI3K, p-AKT, and p-mTOR proteins was significantly increased (P < 0.05). Furthermore, compared with the model group, the expression of SOX9, type II collagen, and Beclin1 proteins in the cartilage tissue of rats in the metformin group was significantly increased (P < 0.05), while the expression of ADAMTS5, P62, as well as p-PI3K, p-AKT, and p-mTOR proteins was significantly decreased (P < 0.05). To conclude, Metformin can improve the autophagy activity of chondrocytes and reduce the degradation of cartilage matrix in osteoarthritis rats by inhibiting the activation of PI3K/AKT/mTOR signaling pathway, thus exerting a protective effect on articular cartilage. Figures and Tables | References | Related Articles | Metrics

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Molecular mechanisms of ligament flavum hypertrophy: analysis based on methylation sequencing and transcriptome integration  He Yang, Tang Buyuan, Lu Changhuai 2025, 29 (5):  1013-1020.  doi: 10.12307/2025.291 Abstract ( 205 )   PDF (2167KB) ( 68 )   Save BACKGROUND: Ligament flavum hypertrophy is the main cause of lumbar spinal stenosis, which is the result of multiple pathological factors working together. Currently, the molecular mechanism and pathway of action of ligament flavum hypertrophy are unclear, and there is a lack of effective non-surgical treatment options.  OBJECTIVE: To investigate the molecular mechanisms of ligament flavum hypertrophy using methylation sequencing and transcriptome integration analysis methods.  METHODS: Five normal ligament flavum tissue samples and five hypertrophic ligament flavum tissue samples were collected. Abnormal methylation sites and methylation status were recorded by methylation sequencing and abnormally expressed genes were recorded by transcriptome integration analysis.  The genes that showed a negative correlation between methylation level and expression level at the intersection of the two were selected. GO and KEGG enrichment analyses were used to study the major functional pathways and molecular functions of differentially expressed genes. Key genes regulating ligamentum flavum hypertrophy were screened using protein-protein interaction analysis. RESULTS AND CONCLUSION: Methylation sequencing of the two groups of the ligament flavum showed 37 173 hypermethylation sites and 10 583 low methylation sites. Transcriptome integration analysis found 720 abnormally expressed genes, of which 463 were upregulated and 257 were down-regulated. There were 383 overlapping genes, of which 192 genes showed a negative correlation between the methylation level and the expression level. GO functional pathway analysis results showed that molecular function was enriched to 10 terms, cellular component was enriched to 15 terms, and biological process (BP) was enriched to 30 terms. The results of KEGG pathway enrichment analysis showed that 192 genes were mainly enriched to 9 pathways, such as PI3K-Akt signaling pathway, Rap1 signaling pathway, and focal adhesion signaling pathway. The protein-protein interaction analysis identified five genes, PPARG, EGFR, CNR1, TNF and COL11A2, which may be the key genes that regulate ligamentum flavum hypertrophy, and they can influence the occurrence and development of ligamentum flavum hypertrophy mainly through the regulation of tissue fibrosis, cell proliferation and differentiation, inflammatory factor levels, and collagen fiber expression. Figures and Tables | References | Related Articles | Metrics

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Relationship between vitamin D levels and reproductive characteristics and exercise dietary situation in postmenopausal women  Wang Dongyang, Yang Qiaohui, Lin Xinchao 2025, 29 (5):  1021-1025.  doi: 10.12307/2025.278 Abstract ( 268 )   PDF (789KB) ( 108 )   Save BACKGROUND: Studies have demonstrated that postmenopausal osteoporosis is related to female reproductive characteristics and exercise diets, but few studies have demonstrated whether female reproductive characteristics and exercise diets have an effect on vitamin D in postmenopausal women. OBJECTIVE: To investigate the relationship of vitamin D levels with female reproductive characteristics and exercise diets and their influencing factors in postmenopausal women in Beijing. METHODS: Totally 727 postmenopausal women with an age range of 46-75 years old who received on-site questionnaires in 17 communities of Beijing from September 2017 to May 2018 were selected as the study subjects, and the questionnaires included the subjects’ basic information and history of menstruation, menopause, pregnancy, and exercise diet. An electrochemiluminescence immunoassay analyzer and its auxiliary reagents were used to determine 25-(OH)D levels. Bone mineral density and T values of the lumbar spine (L1-L4, whole) and both hips (femoral neck, whole) were determined using a dual-energy X-ray bone mineral density detector. The correlation of vitamin D with reproductive characteristics and exercise diet was observed, as well as the influencing factors of vitamin D were analyzed.  RESULTS AND CONCLUSION: There were 136 cases (18.7%) in the vitamin D normal group, 389 cases (53.5%) in the vitamin D insufficient group, and 202 cases (27.8%) in the vitamin D deficient group. The mean vitamin D level was (15.60±5.85) ng/mL. With the increase of vitamin D level, the bone mineral density value and T value of different parts of the body also increased. Vitamin D level was positively correlated with age at menarche, days of menstrual duration, stage of menopause, activity, diet type, and dietary preference (P < 0.05); was negatively correlated with menstrual cycle, age at menopause, and number of childbearing (P < 0.05); and had no correlation with age at first conception and number of pregnancies (P > 0.05). The results of multifactorial ordered Logistic regression analyses showed that there was a positive correlation between the frequency of drinking dairy products and vitamin D level (P < 0.05), and dairy products were a protective factor for vitamin D level. To conclude, vitamin D levels are generally insufficient and bone mineral density values are generally low in postmenopausal women in Beijing. Vitamin D levels are correlated with some reproductive characteristics and exercise diets, and drinking dairy products is a protective factor. Therefore, it is possible to intervene in the dietary situation of postmenopausal women by means of health education about osteoporosis and by increasing vitamin D levels in order to increase bone density values and reduce the prevalence of osteoporosis in the postmenopausal period. Figures and Tables | References | Related Articles | Metrics

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Effects of wogonin on joint inflammation in collagen-induced arthritis rats via the endoplasmic reticulum stress pathway Wang Yuru, Li Siyuan, Xu Ye, Zhang Yumeng, Liu Yang, Hao Huiqin 2025, 29 (5):  1026-1035.  doi: 10.12307/2025.208 Abstract ( 187 )   PDF (2335KB) ( 125 )   Save BACKGROUND: Rheumatoid arthritis is an inflammatory disease. Many studies have shown that wogonin has a good anti-inflammatory effect on rheumatoid arthritis, but its exact efficacy and specific mechanism of action remain to be clarified. OBJECTIVE: To investigate the mechanism of wogonin ameliorating joint inflammation by regulating endoplasmic reticulum stress pathway in rats with collagen-induced arthritis. METHODS: (1) At the animal level: Female Wistar rats were divided into healthy control group, arthritis model group and wogonin treatment group. Rat models of arthritis in the latter two groups were established by subcutaneous injection of bovine type II collagen and adjuvant. In the wogonin group, wogonin was given by gavage for 28 consecutive days after modeling. During this period, the rats in each group were weighed, and arthritis score and ankle swelling were measured every 7 days. After the experiment, the pathological changes of the joint were observed, the mRNA and protein levels of endoplasmic reticulum stress pathway GRP78 and CHOP were detected by qRT-PCR, western blot, and immunohistochemistry. (2) At the cellular level, cell counting kit-8 was used to detect the cytotoxic effect of wogonin on fibroblast-like synoviocytes from rats with collagen-induced arthritis. The fibroblast-like synoviocytes induced by thapsigargin were treated with different concentrations of wogonin. The levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant were detected by ELISA, and the intracellular reactive oxygen species in each group were determined by DCFH-DA probe method. The mRNA and protein levels of GRP78, IRE1α, XBP1s and CHOP were detected by qRT-PCR and western blot, respectively. RESULTS AND CONCLUSION: Compared with the healthy control group, arthritis index score and ankle swelling degree in the arthritis model group were increased (P < 0.01), synovial hyperplasia, inflammatory cell infiltration, cartilage destruction and bone erosion were observed in pathological sections, and the mRNA and protein expressions of GRP78 and CHOP in the ankle were significantly increased (P < 0.01), which were mainly located in synovial tissue and articular surface. Compared with the arthritis model group, the arthritis index score and ankle swelling degree in the wogonin treatment group were decreased (P < 0.05), synovial hyperplasia and the number of inflammatory cells were decreased, cartilage destruction and bone erosion were alleviated, the mRNA and protein expression levels of GRP78 and CHOP in the ankle were decreased (P < 0.05), particularly in synovial tissue and on the articular surface. There was no significant difference in body mass among the three groups (P > 0.05). In the cell experiment, 200 μmol/L wogonin significantly reduced the survival rate of fibroblast-like synoviocytes (P < 0.01). Compared with the blank control group, the levels of interleukin-1β, tumor necrosis factor-α, content of reactive oxygen species, and mRNA and protein expression of GRP78, IRE1α, XBP1s, and CHOP in the thapsigargin group were significantly increased (P < 0.05); compared with the thapsigargin group, 50 and 100 μmol/L wogonin significantly reduced the levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant (P < 0.05, P < 0.01), and 100 μmol/L wogonin significantly reduced the content of reactive oxygen species (P < 0.01) and down-regulated the mRNA and protein expression levels of GRP78, IRE1α, XBP1s and CHOP (all P < 0.05). These results suggest that wogonin can effectively alleviate joint inflammatory responses in rats with collagen-induced arthritis, and the endoplasmic reticulum stress pathway may be the key target of its intervention. Figures and Tables | References | Related Articles | Metrics

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Treating acute type III-V acromioclavicular joint dislocation with single tunnel fixation versus tunnel-free suspension fixation of the coracoid process under shoulder arthroscopy  Zeng Yongtao, Zheng Hongcheng, Nacikedaoerji, Refati·Nijiati, Shu Li, Liu Xu, Chen Hongtao 2025, 29 (5):  1036-1042.  doi: 10.12307/2025.295 Abstract ( 170 )   PDF (1483KB) ( 129 )   Save BACKGROUND: At present, there are few reports on the postoperative efficacy of arthroscopic coracoid tunnel-free suspension fixation and coracoid single tunnel fixation in the treatment of acromioclavicular joint dislocation at home and abroad. The specific clinical efficacy of the two procedures and whether there are other risks need to be explored. OBJECTIVE: To compare the short-term postoperative clinical efficacy of arthroscopic TightRope band plate fixation with single tunnel fixation of the coracoid process and tunnel-free suspension fixation of the coracoid process in the treatment of acute type III-V acromioclavicular joint dislocation. METHODS: A retrospective analysis was performed in 45 patients with acromioclavicular joint dislocation who met the inclusion criteria admitted to the Sixth Affiliated Hospital of Xinjiang Medical University from June 2019 to September 2022, and were divided into coracoid single tunnel fixation group (20 cases) and coracoid tunnel-free suspension fixation group (25 cases) according to the surgical treatment plan. Operation time, incision length, blood loss, Constant-Murley score, visual analogue scale score, the American Shoulder and Elbow Surgeons (ASES) score and intraoperative and postoperative complications of the shoulder joint before operation, 3 months after surgery and the last follow-up were compared between the two groups. RESULTS AND CONCLUSION: All patients successfully completed the operation, and there was no important nerve or blood vessel damage during the operation. The operation time of the coracoid tunnel-free suspension fixation group was significantly shorter than that of the coracoid tunnel-free suspension fixation group (P < 0.05). There was no significant difference in intraoperative blood loss and incision length between the two groups (P > 0.05). All patients were followed up for 12 to 24 months, with an average of (15.29±2.73) months. In the coracoid single tunnel fixation group, at 3 months after operation and the final follow-up, the visual analogue scale score was significantly lower than the preoperative score (P < 0.05); Constant-Murley score and ASES score were significantly increased compared with the preoperative values (P < 0.05). In the coracoid tunnel-free suspension fixation group, at 3 months after operation and the final follow-up, the visual analogue scale score was significantly lower than the preoperative score (P < 0.05); the Constant-Murley score and the ASES score were both significantly higher than the preoperative scores (P < 0.05). At 3 months after operation, the Constant-Murley score of the coracoid tunnel-free suspension fixation group was higher than that of the coracoid single tunnel fixation group (P < 0.05), while there was no significant difference in visual analogue scale and ASES scores between the two groups (P > 0.05). There was also no significant difference in the visual analogue scale, Constant-Murley, and ASES scores between the two groups at the corresponding time points before surgery and at the final follow-up (P > 0.05). Intraoperative and postoperative complications: In the coracoid single tunnel fixation group, there was one case of coracoid cortical rupture and fracture during the tunnel drilling during the operation, and one case of a loss of reduction at 3 months after operation, which was repositioned and fixed with hook plate transposition of the coracoacromial ligament. All patients had good acromioclavicular joint function recovery and no re-dislocation at the final follow-up. All patients in the coracoid tunnel-free suspension fixation group did not suffer from coracoid fractures, loss of reduction and other complications during surgery, postoperatively and at the last follow-up. To conclude, these two arthroscopic treatments for acute type III-V acromioclavicular joint dislocation have the advantages of less trauma, reliable reduction and fixation, and good recovery of shoulder joint function after operation. However, compared with the coracoid single tunnel technique, the coracoid tunnel-free suspension fixation requires shorter time, faster recovery of shoulder joint function in the short term, and avoids the establishment of bone tunnels on the coracoid process, which reduces the probability of iatrogenic fracture of the coracoid process during operation and provides a higher degree of safety. Figures and Tables | References | Related Articles | Metrics

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Evaluation of FTA-LAMP direct extraction method for extracting DNA from Streptococcus mutans  Wang Yuehui, Shang Jin, Yang Chen, Fu Dongge, Cao Can, Zhang Xiaodong, Wang Jingfu 2025, 29 (5):  1040-1049.  doi: 10.12307/2025.279 Abstract ( 198 )   PDF (1564KB) ( 133 )   Save BACKGROUND: Streptococcus mutans is an important pathogen of dental caries, and timely detection of its levels is of great significance for early detection and treatment of dental caries.  OBJECTIVE: To evaluate the effect of loop-mediated isothermal amplification (FTA-LAMP) direct extraction of Streptococcus mutans DNA.  METHODS: (1) Bacterial suspensions containing ATCC standard strains (Streptococcus mutans) were prepared and inoculated into the brain-heart leachate medium. After mixed thoroughly, the mixture was then diluted in a 10-fold gradient into seven concentrations (4.2×107, 4.2×106, 4.2×105, 4.2×104, 4.2×103, 4.2×102, 4.2×10 CFU/ mL), two parallel controls were made for each dilution level, and sterile water was used as a blank control. (2) The DNA of Streptococcus mutans was extracted using FTA Elute card, boiling method, kit extraction and lysate extraction methods separately and then amplified using LAMP technology was amplified. A specificity test was also performed to compare the differences between the four DNA extraction methods.   RESULTS AND CONCLUSION: The DNA extracted by all four methods met the requirements for LAMP amplification. Specificity test results showed that only Streptococcus mutans could specifically amplify the target gene. The detection limit value of the DNA concentration was 4.2×103 CFU/mL for the lysate method, 4.2×104 CFU/mL for the FTA Elute card extraction method, 4.2×106 CFU/mL for the kit extraction method, and 4.2×107 CFU/mL for the boiling method. In the other aspects of the four extraction methods, the kit extraction method had the highest experimental cost, number of steps and time; the other three methods had the same number of steps, with the FTA Elute card method requiring the least amount of instruments, the boiling method having the lowest single cost, and the lysate extraction method taking the least amount of time. Only a small amount of bacteria were needed for successful extraction using both the FTA Elute card and lysate extraction methods. Compared with the FTA Elute card method, the lysate extraction method was superior in terms of time, but it had a high single cost and required more equipment. To conclude, the FTA-LAMP technology established in this study has the advantages of ease of operation, high specificity, high sensitivity, and visualization, which is expected to be a new way for efficient extraction and detection of Streptococcus mutans.   Figures and Tables | References | Related Articles | Metrics

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Effect of balance training with different visual conditions on proprioception in patients with chronic ankle instability  Wu Yihan, Liu Zhongqiang, Wei Qiaoye, Liu Mingdong, Chen Keyi, Li Zhigang 2025, 29 (5):  1050-1057.  doi: 10.12307/2025.286 Abstract ( 356 )   PDF (1059KB) ( 231 )   Save BACKGROUND: Stroboscopic visual training can force sensory reweighting to restore the original weights by increasing sensitivity to proprioceptive information, which may be an effective method to improve proprioception. OBJECTIVE: To determine the effects of balance training in three conditions, low frequency, high frequency and normal vision, on ankle proprioception in patients with chronic ankle instability. METHODS: Thirty-six patients with chronic ankle instability recruited from the students of Southwest Medical University were randomly assigned to a low-frequency vision training group, a high-frequency vision training group, and a normal vision training group, with 12 subjects in each group. Subjects in the three groups underwent progressive hop stabilization and balance training, in which the low-frequency vision training group and the high-frequency vision training group wore stroboscopic spectacles during the training, with a stroboscopic frequency of 1.75 and 5 Hz, respectively. The training in each group was performed three times a week for 4 consecutive weeks. Assessments, including ankle proprioception, ankle stability self-assessment and dynamic postural stability, were performed before training and within 1 week after the completion of training.  RESULTS AND CONCLUSION: There was a significant main effect of time factor in ankle proprioception (P < 0.05). Compared with the pre-training period, subjects in the low-frequency vision training group and the high-frequency vision training group showed significant improvement in ankle proprioception after 4 weeks of training (P < 0.05); and subjects in the low-frequency vision training group showed a significant improvement in ankle proprioception compared with that of the normal vision training group after 4 weeks of training (P < 0.05). There were significant main effects of time factor and group×time interaction in ankle proprioception (P < 0.05). Compared with the pre-training period, the ankle stability self-assessment in all three groups was improved after 4 weeks of training (P < 0.05). And the ankle stability self-assessment in high-frequency visual training group was higher than that in normal vision training group after 4 weeks of training (P < 0.05). Compared with the pre-training period, subjects in the low-frequency vision training group and the high-frequency vision training group showed significant improvements in forward dynamic postural stability, posteromedial dynamic postural stability, and posterolateral dynamic postural stability after 4 weeks of training (P < 0.05), while in the normal vision training group, forward dynamic postural stability and posterolateral dynamic postural stability were significantly improved after 4 weeks of training (P ≤ 0.05). To conclude, balance training under stroboscopic visual conditioning improves proprioception, ankle stability self-assessment, and dynamic postural stability in patients with chronic ankle instability regardless of frequency.  Figures and Tables | References | Related Articles | Metrics

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Correlations between gastrocnemius morphology parameters and physical activity capacity in elderly females under high-frequency ultrasound  Wen Zixing, Xu Xin, Zhu Shengqun 2025, 29 (5):  1058-1063.  doi: 10.12307/2025.285 Abstract ( 195 )   PDF (1097KB) ( 121 )   Save BACKGROUND: The application of high-frequency ultrasound technology provides an effective tool for the precise assessment of skeletal muscle morphology in the elderly. However, the correlation between the morphological parameters of skeletal muscle obtained and physical activity capacity remains unclear. OBJECTIVE: To explore the correlation between morphological parameters of the gastrocnemius muscle and physical activity capacity in elderly females using high-frequency ultrasound imaging technology, thereby identifying effective predictive indicators for physical activity capacity in the elderly. METHODS: Fifty-nine elderly female subjects over the age of 60 with the ability to live independently were recruited in the communities surrounding Shanghai Sanda University. High-frequency ultrasound images of the subjects’ gastrocnemius muscles were collected to obtain the relevant parameters, including muscle thickness, fiber length, pennation angle, and fiber length/muscle thickness (Lf/Tm) index. Physical activity capacity tests were also conducted and relevant indicators included the 10-meter walk test, timed up-and-go test, 30-second chair stand test, and grip strength test. Correlation analyses were performed between various morphological parameters and physical activity capacity test indicators. RESULTS AND CONCLUSION: Significant correlations were found between various muscle morphological parameters (P < 0.05). The pennation angle showed significant correlations with the 10-meter walking speed (r=-0.35, P < 0.05) and timed up-and-go test results (r=0.32, P < 0.05). The Lf/Tm index was positively correlated with 10-meter walking speed and grip strength test results (r=0.39, P < 0.01; r=0.30, P < 0.05), but was negatively correlated with timed up-and-go test results (r=-0.32, P < 0.05). All these findings indicate that the pennation angle and Lf/Tm index of the gastrocnemius muscle show a good correlation with physical activity capacity in elderly females, which can serve as effective predictive indicators for physical activity capacity. Figures and Tables | References | Related Articles | Metrics

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Mechanical stress regulates apoptosis in vascular smooth muscle cells  Xu Fei, Yan Jinqiang, Chai Shoudong 2025, 29 (5):  1064-1072.  doi: 10.12307/2025.309 Abstract ( 340 )   PDF (1027KB) ( 551 )   Save BACKGROUND: With the development of biomechanics, its research into cardiovascular diseases has become more and more extensive. By studying the mechanical properties of blood vessels, the pathogenesis of cardiovascular diseases such as atherosclerosis and restenosis can be effectively revealed and new ideas and methods can be developed for the treatment of cardiovascular diseases. OBJECTIVE: To review the research status of apoptosis of vascular smooth muscle cells induced by mechanical stress and search for potential target molecules and signaling pathways for clinical treatment, thereby improving the clinical treatment effect on cardiovascular diseases such as atherosclerosis and restenosis. METHODS: We searched the literature in CNKI, PubMed and ScienceDirect databases from January 1992 to May 2023. The search terms were “vascular smooth muscle cell, mechanical stress, shear stress, stretch stress, apoptosis” in Chinese and English. Finally, 63 articles were included for review and analysis. RESULTS AND CONCLUSION: Physiological and pathological apoptosis of vascular smooth muscle cells is an adaptive remodeling in response to the changes in vascular mechanics. Vascular smooth muscle cells in different parts have different mechanical stimuli and their pathogenesis is also different. Low shear stress, physiological shear stress and high shear stress directly interact with surface molecules, receptors and proteins of vascular smooth muscle cells to regulate apoptosis-related signaling molecules and inhibit cell proliferation, thus regulating the apoptosis of vascular smooth muscle cells. In this part, the research on promoting proliferation is not summarized. Low stretch stress, physiological stretch stress and high stretch stress can all cause apoptosis of vascular smooth muscle cells, but it is still controversial. There are many mechanoreceptors (such as integrins and receptor tyrosine kinases) on the surface of vascular smooth muscle cells, which can transform mechanical signals into intracellular chemical signals (such as the Hippo pathway), activate the apoptosis signals of vascular smooth muscle cells and regulate the apoptosis of vascular smooth muscle cells. In short, different mechanical stimuli start a variety of signal pathways and regulate the apoptosis of vascular smooth muscle cells through various signal molecules. For example, shear stress affects Fas/FasL and Akt pathways mainly by stimulating prostaglandin secretion and transforming growth factors. Strech stress mainly regulates the YAP pathway and Notch pathway through Yes-related proteins. At different times or intensities, these molecules may play opposite two-way roles. For example, when mouse vascular smooth muscle cells are stretched at 10% physiological tension for 1 hour, cell proliferation increases. However, the proliferation of human vascular smooth muscle cells can decrease after 12 hours of stretching. Clinically, the key molecules of mechanical transduction can be disturbed by searching for key molecules that interfere with mechanical transduction at their critical time points of action. Figures and Tables | References | Related Articles | Metrics

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Physical activity and cognition in older adults: research hotspot and topic evolution  Li Huijun, Li Huangyan, Zhang Yeting 2025, 29 (5):  1073-1080.  doi: 10.12307/2025.301 Abstract ( 293 )   PDF (1558KB) ( 265 )   Save BACKGROUND: In recent years, there has been an explosion of research in the field of physical activity and cognition of older adults, and the research hotspots and topics in this field are constantly evolving. However, a comprehensive review of the literature in this field is lacking. OBJECTIVE: To explore the current international research hotspots and contents in the field of physical activity and cognition of older adults using bibliometrics. METHODS: The Web of Science Core Collection Database, including SCI-EXPANDED, SSCI, A&HCI, CPCI-S, CPCI-SSH, BKCI-S, BKCI-SSH, ESCI, CCR-EXPANDED, IC, etc., was searched for relevant literature in English. CiteSpace software was used to visualize and analyze 2593 documents collected in the Web of Science database. RESULTS AND CONCLUSION: The evolution of the topics of physical activity and cognition of older adults includes five stages: research on companion robots for older adults, research on the risk of diseases such as dementia, research on cognitive ability and its related ability, research on the relationship between physical activity level and cognitive ability in older adults, and research on different intervention methods and their mechanisms. The research in this field tends to be diversified. On the basis of the research on diseases and cognitive risk reduction, more attention has been paid to the effects of different physical activity modalities on cognition and the related mechanisms, which is the current research hotspot and will be the main research trend in the future. Figures and Tables | References | Related Articles | Metrics

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Causal relationship between immune cells and knee osteoarthritis: a two-sample bi-directional Mendelian randomization analysis  Wu Guangtao, Qin Gang, He Kaiyi, Fan Yidong, Li Weicai, Zhu Baogang, Cao Ying 2025, 29 (5):  1081-1090.  doi: 10.12307/2025.292 Abstract ( 365 )   PDF (3520KB) ( 303 )   Save BACKGROUND: Knee osteoarthritis (KOA) is a common chronic inflammatory disease that causes damage to joint cartilage and surrounding tissues. Immune cells play an important role in the immune-inflammatory response in knee osteoarthritis, but the specific mechanisms involved are still not fully understood.  OBJECTIVE: To evaluate the potential causal relationship between 731 immune cell phenotypes and the risk of knee osteoarthritis using Mendelian randomization.  METHODS: Summary statistics of genome-wide association studies (GWAS) for 731 immune cell phenotypes (from GCST0001391 to GCST0002121) obtained from the GWAS catalog and GWAS data for knee osteoarthritis from the IEUGWAS database (ebi-a-GCST007090) were used. Inverse variance-weighted method, MR-Egger regression, weighted median method, weighted mode method, and simple mode method were employed to investigate the causal relationship between immune cells and knee osteoarthritis. Sensitivity analyses were conducted to assess the reliability of the Mendelian randomization results. Reverse Mendelian randomization analysis was also performed using the same methods.  RESULTS AND CONCLUSION: The forward MR analysis indicated significant causal relationships (FDR < 0.20) between knee osteoarthritis and four immune cell phenotypes, namely CD27 on CD24+CD27+ in B cells (OR=1.026, P=0.000 26, Pfdr=0.18), CD33 on CD33dim HLA DR- in myeloid cells (OR=1.014, P=0.000 50,  Pfdr=0.18), and CD45RA+CD28-CD8br %CD8br in Treg cells (OR=1.001, P=0.000 78, Pfdr=0.18), and PDL-1 on monocytes in mononuclear cells (OR=0.952, P=0.000 98, Pfdr=0.18). These immune cell phenotypes showed direct positive or negative causal associations with the risk of knee osteoarthritis. Reverse Mendelian randomization analysis revealed no significant causal relationships (FDR < 0.20) between knee osteoarthritis as exposure and any of the 731 immune cell phenotypes. The results of sensitivity analysis show that the P-values of the Cochran’s Q test and the MR-Egger regression method for bidirectional Mendelian randomization were both greater than 0.05, indicating that there is no significant heterogeneity and pleiotropy in the causal effect analysis between immune cell phenotypes and knee osteoarthritis. To conclude, there may be four potential causal relationships between immune cell phenotypes, such as CD27 on CD24+CD27+ cells, CD33 on CD33dim HLA DR- cells, CD45RA+CD28-CD8br %CD8br cells, and PDL-1 on monocytes, and knee osteoarthritis. These findings provide valuable clues for studying the biological mechanisms of knee osteoarthritis and exploring early prevention and treatment strategies. They also offer new directions for the development of intervention drugs. Figures and Tables | Related Articles | Metrics

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Screening of biomarkers for fibromyalgia syndrome and analysis of immune infiltration Liu Yani, Yang Jinghuan, Lu Huihui, Yi Yufang, Li Zhixiang, Ou Yangfu, Wu Jingli, Wei Bing 2025, 29 (5):  1091-1100.  doi: 10.12307/2025.288 Abstract ( 317 )   PDF (1920KB) ( 199 )   Save BACKGROUND: Fibromyalgia syndrome, as a common rheumatic disease, is related to central sensitization and immune abnormalities. However, the specific mechanism has not been elucidated, and there is a lack of specific diagnostic markers. Exploring the possible pathogenesis of this disease has important clinical significance.  OBJECTIVE: To screen the potential diagnostic marker genes of fibromyalgia syndrome and analyze the possible immune infiltration characteristics based on bioinformatics methods, such as weighted gene co-expression network analysis (WGCNA), and machine learning.  METHODS: Gene expression profiles in peripheral serum of fibromyalgia syndrome patients and healthy controls were obtained from the gene expression omnibus (GEO) database. The differentially co-expressed genes were screened in the expression profile by differential analysis and WGCNA analysis. Least absolute shrinkage and selection operator (LASSO) and support vector machine -recursive feature elimination (SVM-RFE) machine learning algorithm were further used to identify hub biomarkers, and draw receiver operating characteristic curve (ROC) to evaluate the accuracy of diagnosing fibromyalgia syndrome. Finally, single sample gene set enrichment analysis (ssGSEA) and gene set enrichment analysis (GSEA) were used to evaluate the immune cell infiltration and pathway enrichment in patients with fibromyalgia syndrome.  RESULTS AND CONCLUSION: Eight down-regulated differentially expressed genes (DEGs) were obtained after differential analysis of the GSE67311 dataset according to the conditions of log2|(FC)| > 0 and P < 0.05. After WGCNA analysis, 497 genes were included in the module (MEdarkviolet) with the highest positive correlation (r=0.22, P=0.04), and 19 genes were included in the module (MEsalmon2) with the highest negative correlation (r=-0.41, P=6×10-5). After intersecting DEGs and the module genes of WGCNA, seven genes were obtained. Four genes were screened out by LASSO regression algorithm and five genes were screened out by SVM-RFE machine learning algorithm. After the intersection of the two, three core genes were identified, which were germinal center associated signaling and motility like, integrin beta-8, and carboxypeptidase A3. The areas under the ROC curve of the three core genes were 0.744, 0.739, and 0.734, respectively, indicating that they have good diagnostic value and can be used as biomarkers for fibromyalgia syndrome. The results of immune infiltration analysis showed that memory B cells, CD56 bright NK cells, and mast cells were significantly down-regulated in patients with fibromyalgia syndrome compared with the control group (P < 0.05), and were significantly positively correlated with the above three biomarkers (P < 0.05). The enrichment analysis suggested that there were nine fibromyalgia syndrome enrichment pathways, mainly related to olfactory transduction pathway, neuroactive ligand-receptor interaction, and infection pathway. The above results showed that the occurrence and development of fibromyalgia syndrome are related to the involvement of multiple genes, abnormal immune regulation, and multiple pathways imbalance. However, the interactions between these genes and immune cells, as well as their relationships with various pathways need to be further investigated. Figures and Tables | References | Related Articles | Metrics