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18 May 2022, Volume 26 Issue 14 Previous Issue   

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Association of bone mineral density and skeletal muscle with fracture risks in postmenopausal women in Inner Mongolia area Lin Jing, A Sileng, Dong Mei 2022, 26 (14):  2133-2137.  doi: 10.12307/2022.472 Abstract ( 383 )   PDF (620KB) ( 44 )   Save BACKGROUND: The increased risk of osteoporotic fracture is independent of bone mineral density, whereas the effects of muscle and fat on the fracture risk have not been quantitatively assessed. OBJECTIVE: To identify the relationship between bone mineral density, muscle and the risk of osteoporotic fracture in postmenopausal women.  METHODS: Clinical data from 1 032 postmenopausal women, aged 40-49 years, who were admitted at the Second Affiliated Hospital of Inner Mongolia Medical University, were collected and analyzed. The bone mineral density and body composition were measured by dual-energy x-ray absorptiometry, and the fracture risks at the major sites in the next 10 years were assessed using the Fracture Risk Assessment Tool (FRAX®), released by the World Health Organization. RESULTS AND CONCLUSION: The mean age of all the subjects was 64 years (range, 40 to 90 years). Mean bone mineral densities of the lumbar spine, femoral neck, and total hip were (0.78±0.16), (0.64±0.14), and (0.76±0.15) g/cm2, respectively. The appendicular lean mass and appendicular lean mass index were (15.9±2.4) kg and (6.57±1.77) kg/m2 respectively. The fracture risk calculated in 10 years by using the FRAX for hip fracture and major fracture was 4.2% (2.8%, 6.9%) and 1% (0.3%, 2.4%), respectively. The appendicular lean mass index showed a negative association with major fracture and hip fracture risks (P < 0.05). All these findings indicate that the appendicular lean mass index associated with an increased risk of a major fracture or hip fracture. Figures and Tables | References | Related Articles | Metrics

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Co-transplantation of acellular allogeneic dermis and autologous split-thickness skin for repairing diabetic foot wound Gao Lei, Qin Xinyuan, Li Tianbo, Wang Shuo, Yu Zeyang, Wang Jiangning 2022, 26 (14):  2138-2143.  doi: 10.12307/2022.473 Abstract ( 521 )   PDF (832KB) ( 85 )   Save BACKGROUND:  In recent years, the combined transplantation of acellular allogeneic dermis and autologous split-thickness skin has achieved good results in burn wound repair at functional sites; however, few reports have documented the application of this technology in the repair of diabetic foot wounds. OBJECTIVE: To evaluate the clinical value of co-transplantation of acellular allogeneic dermis and autologous split-thickness skin in the repair of diabetic foot wound. METHODS: A retrospective analysis was made on the clinical data of 52 patients with diabetic foot wound who were treated with co-transplantation of acellular allogeneic dermis and autologous split-thickness skin (experimental group, n=26) or with autologous split-thickness skin (control group, n=26) between May 2017 and April 2020. The number of postoperative wound infection, skin graft survival rate, reoperation rate, wound healing time and wound recurrence rate during the 1-year follow-up period were compared between the two groups. An approval was obtained from the Ethics Committee of Beijing Shijitan Hospital, Capital Medical University. Informed consent was obtained from all patients and their relatives.  RESULTS AND CONCLUSION: In the control group, eight patients developed infection in the skin graft area after operation, and among them, six patients had skin graft necrosis. After secondary operation, 2 out of the 6 patients healed after dressing treatment. In the experimental group, two patients developed infection after operation, and their wounds failed to be repaired but healed after dressing. The survival rate of skin graft in the experimental group (92.3%) was significantly higher than that in the control group (69.2%; P < 0.05). The reoperation rate of the experimental group was significantly lower than that of the control group (0 vs. 23.1%; P < 0.05). The wound healing time in the experimental group was (16.15±2.68) days, which was significantly shorter than that in the control group [(21.92±3.05) days; t=-7.25, P < 0.05]. The patients in both groups were followed up for 3 months to 1 year after operation. During the follow-up period, two patients in the experimental group and nine patients in the control group were re-hospitalized after wound recurrence. The wound recurrence rate in the experimental group was significantly lower than that in the control group (7.7% vs. 34.6%; P < 0.05). Therefore, compared with autologous split-thickness skin graft, the co-transplantation of acellular allogeneic dermis and autologous split-thickness skin can promote the survival of the skin and shorten the healing time of the wound. The repaired wound is friction-resistant, which reduces the recurrence of diabetic foot wound, even though there is an increase in hospital cost. Figures and Tables | References | Related Articles | Metrics

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Effects of transforming growth factor beta1 and Ras homolog gene family member A on cell morphology and cytoskeleton during chondrocyte differentiation Chen Yuting, He Feiming, Xiang Wei, Wang Chao, Cao Weiwei, Wang Weishan, Liu Wei 2022, 26 (14):  2144-2149.  doi: 10.12307/2022.474 Abstract ( 484 )   PDF (840KB) ( 36 )   Save BACKGROUND: The important pathological change of osteoarthritis is the degeneration of articular cartilage. Transforming growth factor β1 and Ras homolog gene family member A play an important role in maintaining the stability of articular cartilage and the occurrence and development of osteoarthritis, respectively.   OBJECTIVE: To investigate the effects of transforming growth factor-β1 and Ras homolog gene family member A on chondrocyte morphology, cytoskeleton and expression of related factors during chondrocyte differentiation, and the mutual regulation relationship between transforming growth factor-β1, Ras homolog gene family member A and SRY related HMG box-9. METHODS:  Exogenous transforming growth factor β1 at different concentrations was added to stimulate ATDC5 cells to detect the protein expression of Ras homolog gene family member A and SRY related HMG box-9 at different times. Transforming growth factor-β1, LY-364947 (a potent ATP-competitive inhibitor of transforming growth factor-β receptor I) and lysophosphatidic acid (a Ras homolog gene family member A agonist) were used in different combinations to deal with ATDC5 cells for 72 hours. The protein expression levels of Ras homolog gene family member A, SRY related HMG box-9 and transforming growth factor-β were detected, and the changes in cell morphology and cytoskeleton were also observed.   RESULTS AND CONCLUSION: With the increase of transforming growth factor-β1 concentration and time, the expression levels of Ras homolog gene family member A and SRY related HMG box-9 proteins increased significantly (P < 0.001). Compared with the control group, lysophosphatidic acid significantly increased the expression levels of Ras homolog gene family member A and SRY related HMG box-9 protein (P < 0.001), but lysophosphatidic acid treatment had no effect on the protein expression level of transforming growth factor-β1 (P > 0.05). The combination of transforming growth factor-β1 and lysophosphatidic acid significantly increased the protein levels of transforming growth factor-β1, Ras homolog gene family member A, and SRY related HMG box-9 in the treated cells (P < 0.001). LY-364947 decreased the protein levels of RhoA and SRY related HMG box-9 (P < 0.001), and significantly reduced the activation effects of lysophosphatidic acid on Ras homolog gene family member A and SRY related HMG box-9 (P < 0.001). Compared with the control group, after treatment with transforming growth factor-β1, lysophosphatidic acid and their combination, the cell morphology was elongated, the intracellular actin filaments were arranged in a more orderly manner, and the number of actin filaments aggregated at the cell edge was increased. LY-364947 made the morphology of cells become polygonal, the arrangement of actin filaments was disordered, and the actin filaments at the edge of cells decreased. The changes in cell morphology and cytoskeleton by LY-364947+lysophosphatidic acid treatment were similar to those in the LY-364947 treatment group. Therefore, in ATDC5 cells, transforming growth factor-β1 has a superposition effect on Ras homolog gene family member A and SRY related HMG box-9 protein expression in concentration, dose and time. Transforming growth factor-β1 may be the upstream factor of Ras homolog gene family member A and SRY related HMG box-9, regulates the expression of Ras homolog gene family member A and SRY related HMG box-9 to regulate the function of cytoskeleton, and thus participates in the development and progression of osteoarthritis. Figures and Tables | References | Related Articles | Metrics

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C-X-C chemokine receptor type 4 antagonist delays the degeneration of articular cartilage in guinea pigs He Lu, Li Yanlin, Meng Xuhan, Wang Guoliang, Yang Tengyun, Liao Xinyu, Zhou Xiaoxiang, Yang Guang 2022, 26 (14):  2150-2154.  doi: 10.12307/2022.475 Abstract ( 439 )   PDF (905KB) ( 28 )   Save BACKGROUND: Studies have shown that the stromal cell-derived factor 1/C-X-C chemokine receptor type 4 signaling pathway plays an important role in the occurrence and development of osteoarthritis. OBJECTIVE: To explore the effect of C-X-C chemokine receptor type 4 antagonist on the degeneration of articular cartilage in vivo. METHODS: Ninety-six 6-month-old male Hartley guinea pigs were randomly divided into four groups, namely, TN14003 treatment, T140 treatment, AMD3100 treatment group, and blank control group (n=24 per group). Except for the blank control group without any treatment, in the rest three groups, Alzet micro-pumps were directly implanted and fixed under the skin of the back of the guinea pigs, followed by daily injection of TN14003, T140, and AMD3100 drugs at a concentration of 180 mg/L, respectively. After 12 weeks of interventions, the articular cartilage of the knee joint was taken out from guinea pigs for hematoxylin-eosin staining, Safranin-fast green staining, and modified Mankin histological scoring. Immunohistochemical staining was used to detect the expression levels of interleukin-1 and tumor necrosis factor-α. RESULTS AND CONCLUSION: Hematoxylin-eosin staining and Safranin-fast green staining showed that the degree of cartilage degeneration in the TN14003 treatment group was significantly delayed, with the highest Mankin score, followed by T140 treatment group, AMD3100 group and blank control group in turn. There were significant differences in the Mankin scores between the experimental groups (P < 0.05). The results of immunohistochemical staining analysis showed that the positive expression of interleukin-1 and tumor necrosis factor-α in each experimental group was lower than that of the blank control group, among which the expression was lowest in the TN14003 treatment group (P < 0.05). To conclude, these three kinds of C-X-C chemokine receptor type 4 antagonists can all block the stromal cell-derived factor 1/C-X-C chemokine receptor type 4 signaling pathway in vivo, reduce the expression levels of interleukin-1 and tumor necrosis factor-α, and delay cartilage degeneration, among which TN14003 has the best effects. Figures and Tables | References | Related Articles | Metrics

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Effect of panax notoginseng saponins on platelet-rich plasma promoting bone defect healing in rabbits Li Shijie, Ma Liqiong, Xiong Xianmei, Zhang Yan, Chen Zijie, Feng Junming, Gao Yijia, Zeng Zhanpeng 2022, 26 (14):  2155-2160.  doi: 10.12307/2022.476 Abstract ( 463 )   PDF (1013KB) ( 87 )   Save BACKGROUND: Panax notoginseng saponins combined with platelet-rich plasma can up-regulate the expression of factors related to osteogenesis and vascularization, and promote bone healing.  OBJECTIVE: To observe the release of growth factors from platelet-rich plasma after intragastric administration of panax notoginseng saponin and its effects on bone defect healing in rabbits. METHODS: Eighteen New Zealand white rabbits were randomly divided into three groups: PNS group, control group and blank group. PNS group was treated with panax notoginseng saponins by gavage for 2 weeks. Control group was given 10 mL of normal saline by gavage for 2 weeks. Blank group were fed normally. Platelet-rich plasma was obtained by centrifugation in the PNS group together with the control group. After activation, growth factor release was detected by ELISA at different time points (0, 2 hours, 1, 3, 5, and 7 days after activation). One week later, the model of radial bone defect was established in each rabbit. PNS and control groups were implanted with autologous platelet-rich plasma. The bone defect healing of the three groups was compared based on the results from X-ray examination, gross observation, and hematoxylin-eosin staining. The study protocol was approved by the Experimental Animal Ethics Committee of the First Affiliated Hospital of Guangzhou University of Chinese Medicine (approval No. TCMF1-2019062). RESULTS AND CONCLUSION: The release of growth factors: In the PNS group, the release concentrations of vascular endothelial growth factor A on the 7th day, transforming growth factor-β on the 1st day, basic fibroblast growth factor on the 3rd and 5th days after activation were higher than those of the control group (P < 0.01). Bone defect healing: Two months after operation, X-ray examination results showed that better bone healing was observed in the PNS group than the control group, and bone healing in these two groups was significantly better than that in the blank group. Three months after operation, bone defects were healed in all the three groups. Hematoxylin-eosin staining results showed that the trabecular density was higher in the PNS group than the control group, and was worst in the blank group. All these findings indicate that the intervention of Panax notoginseng saponins can up-regulate the concentration of growth factors released from platelet-rich plasma, which has more advantages in promoting the healing of rabbit bone defects than the use of platelet-rich plasma alone. Figures and Tables | References | Related Articles | Metrics

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Regulatory role of curcumin in hydrogen peroxide-induced autophagy in chondrocytes Cao Shuxing, Song Yongzhou, Li Ming, Zhang Hongliang, Zhao Lihui, Ma Wei 2022, 26 (14):  2161-2166.  doi: 10.12307/2022.477 Abstract ( 378 )   PDF (1002KB) ( 148 )   Save BACKGROUND: Curcumin has a good therapeutic effect on osteoarthritis, but the specific mechanism is still unclear. Activation of autophagy can reduce the severity of osteoarthritis.  OBJECTIVE: To investigate the regulatory effect of curcumin on hydrogen peroxide (H2O2)-induced autophagy in chondrocytes.  METHODS: C57 mouse articular chondrocytes were cultured in vitro and randomly divided into control group, model group (treated with H2O2) and curcumin low-, medium- and high-dose groups (10, 20, 40, 80 μmol/L). Model group was treated with H2O2 (1 mmol/L) to simulate oxidative stress in osteoarthritis. In the different curcumin groups, chondrocytes were treated with different concentrations of curcumin for 48 hours, followed by addition of H2O2. Twenty-four hours later, the cells were collected for detection. Cell counting kit-8 assay was used to detect cell viability in each group. Interleukin-6 and tumor necrosis factor-α levels were detected by ELISA. TUNEL staining was used to detect cell apoptosis. The apoptosis rate of each group was detected by flow cytometry. The expression levels of cleaved caspase-3, Bax/Bcl2, Beclin1, LC3-II/I, protein kinase B (Akt) and mammalian target of rapamycin (mTOR) were detected by western blot. The expression of cartilage matrix degradation related genes, including matrix metalloproteinase 13, ADAM metallopeptidase with thrombospondin type 1 motif 5, type II collagen α1, and Aggrecan, were detected by qRT-PCR. RESULTS AND CONCLUSION: Compared with the model group, the activity of chondrocytes was significantly increased after curcumin intervention (P < 0.05). The expression of inflammatory cytokines was significantly decreased (P < 0.05). Apoptosis was significantly decreased (P < 0.05). Apoptosis-related markers, cleaved caspase-3 and Bax/Bcl2 ratio, were significantly decreased (P < 0.05). The expression of autophagy-related markers, LC3-I/II and Beclin1, was significantly increased (P < 0.05). The expression levels of Akt and mTOR were significantly decreased (P < 0.05). qRT-PCR showed that the mRNA expressions of matrix metalloproteinase 13 and ADAM metallopeptidase with thrombospondin type 1 motif 5 were decreased, while the expressions of type II collagen α1 and Aggrecan were increased (P < 0.05). It is suggested that curcumin can reduce the H2O2-induced apoptosis in chondrocytes by promoting autophagy, and this effect may be related to the Akt/mTOR signaling pathway. Figures and Tables | References | Related Articles | Metrics

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Changes in the expression of bromodomain-containing protein 4, an epigenetic molecule, in a rat model of chronic periapical periodontitis Xu Yinghua, Jiang Long, Shi Chun 2022, 26 (14):  2167-2171.  doi: 10.12307/2022.478 Abstract ( 425 )   PDF (1210KB) ( 101 )   Save BACKGROUND: Apical periodontitis is an infectious inflammatory disease of the periapical tissue caused by bacterial infection. Bromodomain-containing protein 4 (BRD4) plays a central role in epigenetic transmission. Studies have shown that BRD4 exerts an important role in inflammation and bone destruction; however, its role in chronic apical periodontitis has not yet been reported. OBJECTIVE: To establish a rat model of apical periodontitis to detect the role of BRD4 in the development of apical periodontitis. METHODS: Thirty Sprague-Dawley rats were selected and randomly divided into five groups, 0-week group, 1-week group, 2-week group, 3-week group, and 4-week group, with six rats in each group. Dental pulp of the left mandibular first molar was exposed by pulpectomy, and they were sacrificed at 0, 1, 2, 3, and 4 weeks postoperatively. After paraformaldehyde fixation, the mandible was removed, and Micro-CT was taken to identify whether the animal model of periapical periodontitis was successfully constructed. Frozen sections were made 1 month after decalcification, and the role of BRD4 in the development of chronic apical periodontitis was detected by immunohistochemistry. RESULTS AND CONCLUSION: The results of Micro-CT showed that widened periodontal ligament and a certain apical shadow appeared in the rat apical periodontitis model at 1-2 weeks postoperatively. The shadow area increased over time and increased significantly at 3 and 4 weeks (P < 0.05). The apical shadow area in the 1-, 2-, 3-, and 4-week groups was significantly higher than that of the 0-week group P < 0.05). However, there was no statistical difference between the 3- and 4-week groups (P > 0.05). Immunohistochemical results showed that the expression of BRD4 in the 1-, 2-, 3-, and 4-week groups was significantly higher than that of the 0-week group (P < 0.05). Highest BRD4 expression appeared in the 2-week group (P < 0.05), but there was no significant difference between the 1- and 4-week groups (P > 0.05). To conclude, BRD4 plays a certain role in the occurrence and development of apical periodontitis, suggesting that BRD4 participates in the development of chronic apical periodontitis. Figures and Tables | References | Related Articles | Metrics

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Parathyroid hormone promotes bone healing in rabbits after free reduction of mandibular condyle fractures Huang Zhicai, Xie Liuqin, Wang Guangsu, Zhang Guoxing, Tang Zhenglong 2022, 26 (14):  2172-2178.  doi: 10.12307/2022.479 Abstract ( 451 )   PDF (1213KB) ( 36 )   Save BACKGROUND: Surgical reduction and internal fixation are used as the main treatments for severe displacement of condylar fracture. If a bone fragment is disintegrated due to the peeling of the external pterygoid muscle, complications such as delayed healing of condylar fracture block may occur after surgery. Therefore, how to promote bone healing after free reduction of condylar fracture is of concern to clinicians in maxillofacial surgery. OBJECTIVE: To study the effect of intermittent administration of parathyroid hormone on bone healing after free reduction of condylar fracture in rabbits. METHODS: Forty-eight New Zealand rabbits were randomly divided into experimental group and control group, 24 rabbits in each group. An experimental model of free reduction and fixation of mandibular condylar fracture was established in rabbits. The experimental group and control group were respectively subcutaneously injected with 20 μg/kg parathyroid hormone and 1 mL of normal saline on the next day after surgery, respectively. The animals were sacrificed 1, 2, 3 and 4 weeks after surgery. Bone samples at the surgical site were taken for bone healing observation. The expression of osteoprotegerin and receptor activator of nuclear factor kappa B ligand (RANKL) in the fracture area was detected by immunohistochemical staining and real-time fluorescence quantitative PCR. RESULTS AND CONCLUSION: There were more osteoblasts and new callus formed faster in the fracture area with a higher density in the experimental group. In the first 4 weeks after surgery, the number of osteoclasts in the experimental group was less than that in the control group (P < 0.05). The mean absorbance value and mRNA expression level of osteoprotegerin were higher in the experimental group than the control group within 4 weeks after surgery. The mean absorbance value and mRNA expression level of RANKL were lower in the experimental group than the control group within 4 weeks after surgery (P < 0.05). All these findings indicate that the application of parathyroid hormone on the second day after free reduction of mandibular condylar fracture could up-regulate osteoprotegerin and inhibit RANKL expression in the fracture area at the early postoperative stage, thereby promoting the formation of new bone in the fracture area. Figures and Tables | References | Related Articles | Metrics

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Changes in programmed necrosis pathway in the occurrence and development of periapical periodontitis in a mouse model Liu Jie, Wang Min 2022, 26 (14):  2179-2183.  doi: 10.12307/2022.480 Abstract ( 415 )   PDF (941KB) ( 70 )   Save BACKGROUND: Programmed necrosis is related to many inflammatory diseases, but there are few studies on its relationship with oral diseases, and the research on its relationship with apical periodontitis has not been reported. OBJECTIVE: To explore the changes of programmed necrosis pathway in apical periodontitis in a mouse model. METHODS: Thirty 12-week-old male balb/c mice were randomly divided into control group and experimental group according to the random number table method. After 1 week of acclimatization, the experimental group underwent anesthesia to open the bilateral mandibular first molars. To establish a mouse model of periapical periodontitis, the pulp cavity was colonized with concentrated Fusobacterium nucleatum fluid, and sealed with temporary sealing cream. The control group only underwent anesthesia. After 7 days, the mouse mandibles were dissected, and bone resorption was analyzed by Micro-CT. qPCR was used to detect the expression of RIP3 and inflammatory factors, interleukin-1α, interleukin-1β and tumor necrosis factor-α mRNA; and western-blot and immunohistochemical analysis were used to analyze the expression of key molecules RIP3 and pMLKL. The study protocol was approved by the Experimental Animal Ethics Committee of West China School of Stomatology, Sichuan University, with the approval No. WCHSIRB-D-2020-423. RESULTS AND CONCLUSION: Compared with the control group, the experimental group had more periapical bone absorption, and the periapical bone volume fraction and bone density decreased significantly (P < 0.01). Compared with the control group, the experimental group had higher mRNA expression of bone inflammatory factors, including interleukin-1α, interleukin-1β and tumor necrosis factor α, and protein expression of RIP3 and pMLKL in the programmed necrosis pathway. The above results indicate that the occurrence and development of apical periodontitis may be related to the activation of programmed cell necrosis. Figures and Tables | References | Related Articles | Metrics

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Effect of uniaxial fatigue exercise on patellofemoral cartilage injury in a rabbit Tan Xinfang, Guo Yanxing, Qin Xiaofei, Zhang Binqing, Zhao Dongliang, Pan Kunkun, Li Yuzhuo, Chen Haoyu 2022, 26 (14):  2184-2189.  doi: 10.12307/2022.481 Abstract ( 390 )   PDF (977KB) ( 53 )   Save BACKGROUND: There is a high incidence of patellofemoral cartilage injury in clinical practice. However, the current research on its etiology is insufficient. Hyperactivity is one of the pathological mechanisms widely recognized in clinic, and understanding the occurrence and development of patellofemoral injury is of great significance. OBJECTIVE: To study the effect of uniaxial fatigue exercise on the patellofemoral articular cartilage, and to explore patellofemoral cartilage injuries caused by fatigue in rabbits, so as to provide an experimental basis for understanding the effect of hyperactivity on patellofemoral cartilage lesions. METHODS: Eight New Zealand white rabbits were adaptively fed for 1 week. The right knee of each rabbit was selected as the experimental side and the left knee as the control side. The right knee was fixed on a modeling machine for uniaxial fatigue exercise, and the activity angle was set to be 0°-95° and the activity frequency was set at 60 beats per minute, 90 minutes a day, for 2 weeks. The left knee of each rabbit was untreated. After modeling, MRI images of the rabbit knee joints were collected. The animals were then sacrificed and sampled, and the cartilage tissue sections of the patellofemoral joint were observed and assessed by the Mankin score. RESULTS AND CONCLUSION: The patellar cartilage of the experimental side was significantly damaged. After 2 weeks of uniaxial fatigue exercise, the patellar cartilage of the experimental side had dull color, visible fissures, rough surface, and hyperplasia at the edge of the patellofemoral interface, while no obvious cartilage degeneration was observed on the control side. The results of knee MRI showed that the signal intensity of the patellar cartilage on the experimental side was heterogeneous. Hematoxylin-eosin staining results revealed that the cartilage surface of the experimental side was not smooth, and chondrocyte proliferation, disarrangement, and multiple tidal lines were observed under a light microscope. The Mankin score of the experimental side was significantly higher than that of the control side (P < 0.05). These findings indicate that 2-week uniaxial fatigue exercise can cause mild damage to the cartilage of the patellofemoral joint in rabbits, accompanied by pathological changes such as cartilage swelling and fissures. Figures and Tables | References | Related Articles | Metrics

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Correlation between interleukin 23/helper T17 cell axis and lumbar disc herniation Yang Yang, Liu Jiajia, Xue Jianhua, Liu Yunfei, Yao Yu 2022, 26 (14):  2190-2195.  doi: 10.12307/2022.482 Abstract ( 446 )   PDF (825KB) ( 92 )   Save BACKGROUND: For lumbar disc herniation, interleukin-23 promotes the Th17 cells to secrete interleukin-17, and then interleukin-17 cooperates with tumor necrosis factor-α to produce inflammation mediators. It would aggravate inflammation and autoimmune response, and then cause some symptoms such as sciatica.   OBJECTIVE: To explore the association between interleukin-23/Th17 axis and lumbar disc herniation. METHODS:  Thirty-eight samples of nucleus pulposus were selected, of which 30 were taken from patients with lumbar disc herniation (trial group) and 8 from patients with lumbar vertebral fractures (control group). Peripheral blood samples were meanwhile taken from two groups of patients on admission. All patients, who were admitted to the Department of Spine Surgery, Affiliated Hospital of Nantong University, were diagnosed based on clinical symptoms, imaging examinations and intraoperative confirmation. Immunohistochemical method was used to detect the expression of interleukin 23 in the nucleus pulposus tissue, and ELISA assay was used to detect the levels of interleukin 17, interleukin 23, and tumor necrosis factor-α in the nucleus pulposus tissue and peripheral blood. Pearson correlation analysis was then performed.   RESULTS AND CONCLUSION: Immunohistochemistry detection showed that the expression of interleukin-23 was significantly higher in the trial group than the control group (P < 0.01). The levels of interleukin-17, interleukin-23 and tumor necrosis factor-α in the nucleus pulpous and peripheral blood all significantly increased in the trial group compared with the control group (P < 0.01). There was a significant positive correlation between these three cytokines in the nucleus pulposus tissue of the trial group (r > 0.5, P < 0.01). To conclude, lumbar disc herniation is closely related to interleukin-23/Th17 axis inflammatory response. Figures and Tables | References | Related Articles | Metrics

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Establishment and identification of a myeloid-derived growth factor deficiency model in apolipoprotein E knockout mice Ding Yan, Xiang Guangda, Meng Biying, Xu Xiaoli, Chen Yuefu 2022, 26 (14):  2196-2201.  doi: 10.12307/2022.483 Abstract ( 456 )   PDF (816KB) ( 75 )   Save BACKGROUND: There are few studies on myeloid-derived growth factor (MYDGF) and atherosclerosis and metabolic diseases. Therefore, a mouse model of bone marrow specific MYDGF deficiency with apolipoprotein E (ApoE) knockout is particularly important for studying the relationship between MYDGF and atherosclerotic diseases. OBJECTIVE: To establish and identify the mouse model of bone marrow specific MYDGF deficiency with ApoE knockout.  METHODS: ApoEflox/flox mice and bone marrow specific MYDGFflox/fiox mice were purchased from the Shanghai Model Organisms Centre, Inc (Shanghai, China). Five ApoEflox/flox male mice were selected to mate with 10 MYDGFflox/fiox female mice, and 30 F1 progeny mice with genotype of MYDGFflox/+ApoEflox/+ were obtained and mated with each other. Finally 30 mice with genotypes of MYDGFflox/floxApoEflox/flox and 34 ApoEflox/flox progenies were obtained. The MYDGFflox and ApoEflox genotypes were identified by PCR, and the body length and body mass of MYDGFflox/floxApoEflox/flox mice and ApoEflox/flox mice at 2 months were recorded. The expression of MYDGF protein in the mouse bone marrow tissues was detected by western blot assay, and immunofluorescence was used to detect the expression of MYDGF in the mouse bone marrow cells. The plaque area of the thoracic aorta in the mouse was detected by oil red O staining. The study was approved by the Animal Ethic Committee of PLA General Hospital of Central Theater Command. RESULTS AND CONCLUSION: There were 34 ApoEflox/flox mice and 30 MYDGFflox/floxApoEflox/flox mice, with no significant difference in their body length and body mass (both P > 0.05). The relative expression level of MYDGF protein in the bone marrow of MYDGFflox/floxApoEflox/flox mice was significantly lower than that of ApoEflox/flox mice (P < 0.05). The percentage of plaque area in the thoracic aorta of MYDGFflox/floxApoEflox/flox mice was significantly higher than that of ApoEflox/flox mice (P < 0.05). Therefore, MYDGF gene was successfully knocked out in ApoEflox/flox mice, and the homozygous mouse model of bone marrow knockout MYDGF gene in ApoE knockout mice was successfully constructed and identified by genotype and protein tissue levels. To conclude, MYDGF gene deficiency can aggravate atherosclerosis in ApoE knockout mice. Figures and Tables | References | Related Articles | Metrics

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Effects of superoxide dismutase on proliferation and c-myc expression of lung fibroblasts activated by supernatant of silicon dioxide-induced rat lung macrophages Kan Quan, Zhang Yan, Wang Haitao, Li Ran, Tian Yanxia, Lyu Cuiping 2022, 26 (14):  2202-2206.  doi: 10.12307/2022.484 Abstract ( 362 )   PDF (893KB) ( 30 )   Save BACKGROUND: c-Myc is a well-known oncogene overexpressed in many cancers. Alveolar macrophages are important functional cells of the lungs, not only involved in the immune defense of the lungs, swallowing bacterial particles that invade the lungs, but also secreting large amounts of biologically active substances to maintain the normal physiological functions of the lungs and the body. Superoxide dismutase has a close relationship with tumors. OBJECTIVE: To observe the effects of superoxide dismutase on cell proliferation and c-myc expression in lung fibroblasts activated by supernatants of silicon dioxide (SiO2)-induced rat alveolar macrophages.  METHODS: Alveolar macrophages were obtained by in situ alveolar lavage technique to prepare conditional culture supernatant: superoxide dismutase culture supernatant (superoxide dismutase+alveolar macrophages+serum-free DMEM), SiO2 supernatant (SiO2+alveolar macrophages+serum-free DMEM), SiO2+superoxide dismutase culture supernatant (SiO2+superoxide dismutase+alveolar macrophages+serum-free DMEM). The supernatant was collected at 1, 2, 4, 8, 16, and 32 hours after culture. Inducted culture of lung fibroblasts: passage 3 lung fibroblasts were taken and induced by the combination of conditional supernatant and 5% fetal bovine serum-DMEM in a 1:1 ratio. There were five groups in the experiment: negative control group (2.5% fetal bovine serum-DMEM culture), positive control group (10% fetal bovine serum-DMEM culture), superoxide dismutase supernatant group, SiO2 supernatant group, and SiO2+superoxide dismutase supernatant group. Culture time was synchronized with the above time points. MTT, immunocytochemistry and RT-PCR methods were used to detect lung fibroblast proliferation, c-myc protein and mRNA expression. The study protocol was approved by the Animal Experiment Ethics Committee of North China University of Science and Technology. RESULTS AND CONCLUSION: Compared with the control group, cell proliferation and expression of c-myc protein and mRNA in lung fibroblasts were singificantly increased in the SiO2 supernatant group. Treatment with SiO2 and superoxide dismutase could inhibit the elevation of cell proliferation, protein and mRNA levels of c-myc (P < 0.05). To conclude, superoxide dismutase can attenuate fibroblast proliferation and high expression of c-myc in rat lung fibroblasts induced by supernatant of SiO2-treated lung macrophages. Figures and Tables | References | Related Articles | Metrics

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Platelet-rich fibrin combined with induced bone matrix repairs bone defects around oral implants in rabbits Gao Xixin, Wang Xi, Fan Xuhui, Cui Yi, Yang Wei, Zhao Yunzhuan 2022, 26 (14):  2207-2213.  doi: 10.12307/2022.485 Abstract ( 410 )   PDF (1781KB) ( 175 )   Save BACKGROUND: Platelet-rich fibrin and artificial bone materials have been widely used in the repair and regeneration of peri-implant bone defects. However, there was a lack of research on the osteogenesis of the two materials in different proportions. OBJECTIVE: To investigate the effect of platelet-rich fibrin combined with bone matrix on the regeneration of peri-implant bone defects in rabbits.  METHODS: A bone defect model around the oral implant was established in 12 large-ear white rabbits. Three cylindrical bone defect areas with a diameter of 5 mm and a depth of 2 mm were prepared along the lower edge of the right mandible, which were numbered 1-3 from the mesial to the distal. After placement of titanium screws, the 2:1, 1:1, and 1:2 mixtures of platelet-rich fibrin and bone matrix were used respectively to fill in the defects. Another three same bone defects were prepared along the lower edge of the left mandible, which were numbered 4-6 from the distal to the mesial. Titanium screw screws were placed, No. 4 defect was filled with nothing as a blank control, No. 5 was filled with platelet-rich fibrin, and No. 6 was filled with bone matrix. Twelve rabbits models were randomized into 4-, 8-, 12-week groups, with 4 rabbits in each group. One rabbit from each group was randomly selected, killed and fluorescently labeled. Tetracycline (25 mg/kg) and calcein (5 mg/kg) were subcutaneously administered at 10 and 3 days before death, respectively. Other animals were killed at 4, 8, and 12 weeks after modeling, and the osteogenic effect was statically analyzed by general observation, hematoxylin-eosin staining, fluorescent labeling, and methylene blue/acid fuchsin staining.  RESULTS AND CONCLUSION: Bone formation rate from high to low was: platelet rich fibrin/bone matrix 2:1 > platelet rich fibrin > platelet rich fibrin/bone matrix 1:1 > platelet rich fibrin/bone matrix 1:2 > bone matrix > blank control. Both platelet-rich fibrin and bone matrix have a good effect in bone repairing bone defect. When platelet rich fibrin and medical induced bone matrix are used in combination, the osteogenic effect becomes better with the increase of platelet-rich fibrin concentration. The combined application of platelet-rich fibrin and bone matrix can accelerate bone healing of implants. Figures and Tables | References | Related Articles | Metrics

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Hot spots and frontiers of rehabilitation robot research in recent 10 years: a bibliometric analysis based on the Web of Science database Xue Xiali, Deng Zhongyi, Sun Junzhi, Li Ning, Ren Wenbo, Zhou Ling, He Ye 2022, 26 (14):  2214-2222.  doi: 10.12307/2022.486 Abstract ( 608 )   PDF (1395KB) ( 109 )   Save BACKGROUND: Traditional rehabilitation training has limited potential to improve functional recovery from chronic injuries. Increasing attentions have been paid to the application of rehabilitation robots in rehabilitation training of chronic injuries. OBJECTIVE: To analyze and track the hot spots and frontiers of related research in the field of rehabilitation robot in the past 10 years, thereby providing some guidance for future research. METHODS: The literatures regarding rehabilitation robots published from 2010 to 2020 were retrieved in the Web of Science core database by computer. Search strategy was TS=(rehabilitation robot OR rehabilitation robotics). CiteSpace 5.7 visualization software was used to analyze the hot spots and frontiers of rehabilitation robot research from the aspects of high-influence countries/regions, institutions, authors, high-frequency keywords and burst words. RESULTS AND CONCLUSION: A total of 3 194 literatures were included. In recent years, the research on rehabilitation robots has been growing steadily. The number of relevant literatures published annually shows a steady increase trend. The number of articles published by the United States ranks first, followed by China. Northwestern University in the United States ranks first with 161 articles published. Professor Riener R, from the University of Zurich, Switzerland, has published 48 articles, ranking the first among the authors. Nine representative keyword clusters have formed, and the research emphasis and direction change over time. In recent 10 years, the relevant research focuses on intelligent control of rehabilitation robots, task analysis and learning, performance and reliability, and how to realize the natural and accurate interaction between robot and human through the integration of machine intelligence and biological intelligence. At present, rehabilitation robots are the most widely used in the field of upper limb and nerve injuries, and the interest in brain-machine interface, virtual reality, flexible wearable, task analysis and the exoskeletons has increased in the research of rehabilitation robot, which are the frontiers and hot issues in recent years, representing the development trend of future studies, and referring to the future research direction. Future research in the field of rehabilitation robots should focus on the following aspects: First, focus on the functional needs of patients to improve the quality of life. Secondly, strengthen multidisciplinary cooperation and build a cooperation network among regional countries. Figures and Tables | References | Related Articles | Metrics

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Visualization analysis on research progress and hotspots of exercise therapy for sarcopenia in older adults in recent decade Wang Susu, Li Lifeng, Zhang Yimin 2022, 26 (14):  2223-2230.  doi: 10.12307/2022.487 Abstract ( 498 )   PDF (901KB) ( 100 )   Save BACKGROUND: In addition to reducing personal quality of life, sarcopenia will also have a medical burden to the society. In view of the risk factors causing sarcopenia, corresponding interventions are mainly carried out from two aspects of exercise and nutrition. Especially, exercise intervention is of great significance for the treatment of sarcopenia. OBJECTIVE: To analyze the research status, hotspots and tendency of exercise intervention for the treatment of sarcopenia in older adults. METHODS: Based on the core collection of Web of Science citation index database (Web of Science TM), a cross-search of core studies on exercise intervention for sarcopenia in the past 10 years in the database was conducted, and 2 484 articles were included. Using Citespace5.7.R1 to filter and remove the retrieved data, a scientometric analysis was conducted on 2 401 included literatures.  RESULTS AND CONCLUSION: Increasing concern has been paid to sarcopenia in older adults. The number of international studies on exercise therapy for sarcopenia in older adults increases year by year, and it is estimated that the popularity will not decrease in the next few years. The top three countries with the most publications are the United States, Japan and England, but the inter-regional and inter-institutional cooperation is not obvious. The academic teams with both publication volume and centrality formed with the core of prolific authors include Maastricht University in the Netherlands, McMaster University in Canada and Sacre Coeur Catholic University in Italy. The high-frequency key words include muscle strength, body composition, physical activity, frailty, resistance exercise, nutritional supplement, etc., indicating that sarcopenia in older adults is a complex disease with multiple factors. Resistance training combined with nutritional supplement is an effective intervention means for sarcopenia in older adults. In recent 5 years, the burst keywords include diabetes patients, fracture, heart failure, mice, blood flow restriction, etc., suggesting that sarcopenia in older adults is related to the risk of fission, type 2 diabetes, heart failure and other diseases, and even the prognosis of some diseases. Therefore, the construction of a new model and strategy of nutrition-exercise intervention for sarcopenia with different concurrent diseases will become a hotspot in the future. Resistance training is the core component of exercise intervention, and the combination of low-intensity resistance training and blood flow restriction will have great potential to become a popular intervention in the future. By cluster analysis of the key references, nine clusters have been obtained. Among them, the large clusters with a large number of references include “inflammation,” “leucine,” “autophagy,” “epidemiology,” “fadedness” and “protein,” among which “inflammation” belongs to an emerging cluster. In the past 10 years, studies on the efficacy of exercise in this disease have been mainly carried out at the cellular and molecular levels of tissue engineering, in which the effects of exercise on chronic inflammation and autophagy channels are the basic research topics. Top 10 highly cited literatures are mostly consensus guidelines published by the working groups on senile sarcopenia from various continents, and also focus on sports combined with protein supplement therapy strategy, which are the knowledge base in this field, and reflect the research fields of continuous concerns and future directions that can continue to break through.  Figures and Tables | References | Related Articles | Metrics

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Regulatory mechanism of aerobic exercise on cardiac remodeling in spontaneously hypertensive rats Zhu Zheng, Fu Changxi, Ma Wenchao, Ma Gang, Peng peng 2022, 26 (14):  2231-2237.  doi: 10.12307/2022.488 Abstract ( 605 )   PDF (1146KB) ( 104 )   Save BACKGROUND: Renin-angiotensin system is the main pathophysiological mechanism that mediates the occurrence and development of hypertension. Regular exercise, especially aerobic exercise, can prevent and treat many cardiovascular diseases. However, the optimal exercise prescription for hypertension has not been determined. OBJECTIVE: To observe the effect of aerobic exercise on cardiac remodeling and to investigate the possible mechanism of local and systemic renin-angiotensin system in spontaneously hypertensive rats (SHR) METHODS: Thirty male SHR rats were randomly divided into SHR sedentary group and SHR exercise group. At the same time, 15 Wistar-Kyoto rats were used as normal blood pressure control group (WKY). The animals in the WKY and SHR sedentary groups were caged and raised quietly, and the SHR exercise group performed moderate intensity treadmill exercise for 8 weeks. After the experiment, caudal artery blood pressure was measured by non-invasive sphygmomanometer. Cardiac structure and function were detected by echocardiography. Myocardial histopathology was observed by hematoxylin-eosin and Masson staining. Angiotensin converting enzyme (ACE) and ACE2 activities in serum and heart were measured by fluorescence substrate method, and angiotensin II (Ang II) and Ang(1-7) contents in serum and heart were detected by high performance liquid chromatography. The protein expression of ACE, Ang II type 1 receptor (AT1R), ACE2 and Mas receptor was detected by western blot. The study protocol was reviewed and approved by the Ethics Committee of Xuzhou University of Technology (approval No. XZUTLL 2019-003-02). RESULTS AND CONCLUSION: Cardiac structure and function: compared with the WKY group, blood pressure increased (P < 0.05), left ventricular concentric hypertrophy and myocardial fibrosis occurred (P < 0.05), and cardiac function decreased (P < 0.05) in SHR sedentary group. Compared with the SHR sedentary group, blood pressure decreased (P < 0.05), left ventricle presented eccentric hypertrophy and myocardial fibrosis alleviated (P < 0.05), and cardiac function improved (P < 0.05) in the SHR exercise group. Local (heart) renin-angiotensin system: compared with the SHR sedentary group, cardiac ACE activity and protein expression and Ang II content decreased (P < 0.05), Ang(1-7) content increased (P < 0.05), ACE2 and Mas receptor protein expression upregulated (P < 0.05), ACE/ACE2 activity and protein expression ratio, Ang II/Ang(1-7) content ratio, and AT1R/Mas receptor protein expression ratio decreased (P < 0.05) in the SHR exercise group. Systemic renin-angiotensin system: there was no significant difference in the activity of ACE and ACE2, ACE/ACE2 activity ratio, the content of Ang II and Ang(1-7), and Ang II/Ang(1–7) content ratio of serum in all groups (P > 0.05). To conclude, aerobic exercise regulates local (heart) renin-angiotensin system to shift ACE-Ang II-AT1R axis to ACE2-Ang(1-7)-Mas receptor axis, thereby inhibiting cardiac remodeling in SHR rats. Figures and Tables | References | Related Articles | Metrics

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Methazolamide effects on intraocular pressure, retinal and choroidal thickness in rats with tail suspension for 2 weeks Gong Yubo, Zhang Wenqian, Guo Xiaohua, Yan Jin, Song Feilong, Shi Yuanyuan, Luo Ling, Zhao Jun, Zhao Hongwei 2022, 26 (14):  2238-2242.  doi: 10.12307/2022.489 Abstract ( 402 )   PDF (670KB) ( 32 )   Save BACKGROUND: Weightlessness can affect intraocular pressure and ocular structure changes. Methazolamide can reduce intraocular pressure, but its effect on intraocular pressure, retinal and choroid thickness in weightlessness is rarely reported. OBJECTIVE: To investigate the effect of the methazolamide on intraocular pressure and retinal and choroidal thickness in rats with simulated microgravity for 2 weeks.  METHODS: Sixteen healthy Sprague-Dawley rats were randomly divided into two groups: control group (n=8) and drug group (n=8). A model of simulated microgravity environment was established in each rat by -30° tail suspension method. All the rats were not treated before tail suspension, and intragastrically given normal saline and methazolamide saline solution in the two groups respectively after tail suspension, once a day, for 14 continuous days. iCare tonometer was used to measure the changes of intraocular pressure in tail-suspended rats before tail suspension and 1, 3, 7, and 14 days after tail suspension. EDI SD-OCT was used to measure the changes of retinal and choroidal thickness in tail-suspended rats before tail suspension and 1, 3, 7, and 14 days after tail suspension. The study protocol was approved by the Animal Experiment Ethics Committee of the PLA Strategic Support Force Characteristic Medical Center. RESULTS AND CONCLUSION: Intraocular pressure in the control group increased after tail suspension, which was significantly higher at 14 days after tail suspension than the baseline (P < 0.05) as well as significantly higher at 7 days than 23 days after tail suspension (P < 0.05). In the drug group, there was no significant difference in the intraocular pressure before and after tail suspension (P > 0.05). Compared with the control group, the intraocular pressure was significantly reduced in the drug group (P < 0.05). Retinal thickness showed no significant changes in each group before and after tail suspension (P > 0.05), and there was also no significant difference between the two groups (P > 0.05). In the control group, choroidal thickness was increased after tail suspension, and became thicker at 3 days than 1 day after tail suspension (P < 0.05). However, there was no significant difference at 7 and 14 days after tail suspension (P > 0.05). In the drug group, choroidal thickness was increased after tail suspension, which was significantly increased at 3, 7, 14 days compared with 1 day after tail suspension (P < 0.05). However, there was no significant difference at 3 days and 7, 14 days after tail suspension (P > 0.05). Compared with the control group, the choroidal thickness was significantly reduced in the drug group (P < 0.05). To conclude, 2-week simulated microgravity has a significant effect on the rat’s intraocular pressure. With the extension of tail suspension time, the intraocular pressure is increased and become significantly elevated at 14 days after tail suspension. The use of methazolamide can effectively inhibit the elevation of intraocular pressure. Moreover, 2-week simulated microgravity has no obvious effect on the retinal thickness, but has a significant effect on the choroidal thickness of rats. With the extension of tail suspension time, the choroidal thickness is increased, while the use of methazolamide can effective reduce the increase in choroidal thickness. Figures and Tables | References | Related Articles | Metrics

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Mechanism by which antler glue treats avascular necrosis of the femoral head induced by retinoic acid in rats: a serum proteomics study Hu Yanan, Wang Ping, Du Haitao, Jing Tianyuan, Wang Chengcheng 2022, 26 (14):  2243-2251.  doi: 10.12307/2022.490 Abstract ( 333 )   PDF (1798KB) ( 94 )   Save BACKGROUND: The research group has found that the small molecule peptides of antler gum are rich in peptide chains that promote bone growth, proliferation and ossification of bone marrow mesenchymal stem cells. The specific mechanism and target of antler glue in the treatment of avascular necrosis of the femoral head are still unclear, which needs further studies. OBJECTIVE: To explore the mechanism of antler glue in the treatment of femoral head necrosis based on proteomics. METHODS: Thirty-six female Wistar rats, SPF grade, were randomized into a blank group, a model group, and an antler glue group. The rats in the latter two groups were given retinoic acid 70 mg/kg once a day for 8 weeks to establish a rat model of femoral head necrosis, while the rats in the blank group were not treated. At 8 weeks after modeling, the rats in the antler glue group were given antler glue 0.35 g/kg, and those in the model and blank groups were given the same volume of 0.9% sodium chloride solution, once a day by gavage for 8 weeks. Pathological examination of bone tissue was used for verifying the successful modeling and the repair effect of antler glue on the femoral head. Non-standard (Label-free) proteome quantification technology was used to detect differential genes among groups. Biological function of differential proteins and signaling pathways involved were enriched based on GO and KEGG database analyses. STRING database was used to construct the target protein-protein interaction network diagram. The study protocol was approved by the Animal Experiment Ethics Committee of Shandong Academy of Traditional Chinese Medicine. RESULTS AND CONCLUSION: The pathological sections of bone tissue showed that antler glue could effectively repair the necrotic femoral head. A total of 1 457 kinds of proteins were identified, including 353 kinds of common differential proteins between blank group and model group as well as between model group and antler glue group. In the model group, 97 kinds of differential proteins that increased or decreased showed a significant callback after intervention with antler glue. The mechanism of antler glue in the treatment of femoral head necrosis involves blood circulation, energy metabolism, inflammatory reaction and immune process. Protein disulfide isomerase (P4HB), cadherin 2 (CDH2), annexin A2 (ANXA2), proprotein convertase subtilisin/kexin type 9 (PCSK9), milk fat globule epidermal growth factor 8 (MFGE8), and bone morphogenetic protein may be important targets of antler glue. Antler glue may treat femoral head necrosis by regulating transforming growth factor β, glycolysis/gluconeogenesis, and PI3K-Akt signaling pathways. Figures and Tables | References | Related Articles | Metrics

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Effect of electroacupuncture combined with triptolide on transforming growth factor beta expression in synovium and synovial fluid in a mouse model of osteoarthritis Hu Yihua, Yang Chunhua, Lu Yuanyuan, Sun Deyi 2022, 26 (14):  2252-2258.  doi: 10.12307/2022.491 Abstract ( 469 )   PDF (728KB) ( 58 )   Save BACKGROUND: Traditional Chinese medicine methods for treating knee osteoarthritis include acupuncture and traditional Chinese medicine. Triptolide has anti-inflammatory and anti-cancer effects, and it also has significant effects in treating arthritis. However, its specific mechanism is still unclear. OBJECTIVE: To investigate the effect of electroacupuncture combined with triptolide on the transforming growth factor-β signal pathway related to osteoarthritis.  METHODS: Forty 8-week-old SPF mice were selected and fed for 1 week. Mice were then randomized into five groups: blank control group, model group, electroacupuncture group, triptolide group, and electroacupuncture combined with triptolide group (combined use group). A mouse model of knee osteoarthritis was established using intraarticular injection of monoiodoacetate in the latter four groups. After the model was successfully constructed, the mice in the blank control group and model group were raised normally; the mice in the electroacupuncture group were treated with electroacupuncture to stimulate the knee joints; the mice in the triptolide group were treated with intragastric administration of triptolide; and the mice in the combined use group were given electroacupuncture at the knee joints and intragastric administration of triptolide. Electroacupuncture was given once a day, and triptolide was administered once a day. Treatments in each group lasted for 4 weeks. Pressure-pain thresholds were observed in each group before and after treatment. Inflammation of the knee joint was evaluated by the macro scoring system. The peripheral blood samples of mice were collected to detect the levels of inflammatory factors, tumor transforming factor-α, interleukin-1β and interleukin-6, by ELISA kit. Western blot assay was used to detect the protein expression levels of matrix metalloproteinase 2, matrix metalloproteinase 9, and transforming growth factor β1 in mouse synovium and synovial fluid.  RESULTS AND CONCLUSION: After intervention, compared with the model group, a great improvement in knee osteoarthritis was achieved in the electroacupuncture and triptolide groups (P < 0.05), and their combined use showed a better effect (P < 0.01). After intervention, the pain threshold of mice increased significantly in the electroacupuncture and triptolide groups compared with the model group (P < 0.05), and the pain threshold in the combined use group increased more significantly (P < 0.05). During the treatment, the arthritis score of mice in the model group gradually increased; compared with the model group, the arthritis scores decreased in the electroacupuncture and triptolide groups, and the score of the combined use group had a significant decline. After intervention, both electroacupuncture and triptolide significantly decreased the levels of tumor transforming factor-α, interleukin-1β and interleukin-6 in the peripheral blood of mice compared with the model group (P < 0.05), and their combined use could extremely significantly decrease the levels of these inflammatory factors in the peripheral blood of mice (P < 0.01). Western blot results revealed that after intervention, the expression levels of matrix metalloproteinase 2, matrix metalloproteinase 9, and transforming growth factor β1 were significantly increased in the synovium and synovial fluid of mice in the electroacupuncture group and the triptolide group compared with the model group (P < 0.05), while the expression levels of related proteins were extremely significantly increased (P < 0.01). It is suggested that electroacupuncture combined with triptolide may treat knee osteoarthritis in mice through transforming growth factor β signaling pathway. Figures and Tables | References | Related Articles | Metrics

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Treatment of Achilles tendinitis with an ultrasonic device for emulsification Yang Xiaoxiao, Xu Yuanjing, Li Wentao, Wang Wenhao, Ma Zhenjiang, Wang Jinwu 2022, 26 (14):  2259-2264.  doi: 10.12307/2022.492 Abstract ( 688 )   PDF (956KB) ( 85 )   Save BACKGROUND: At present, conservative and surgical treatments are difficult to cure tendinitis. A minimally invasive and convenient treatment has not been widely used in clinical practice. OBJECTIVE: To explore the feasibility of applying ultrasonic emulsification device to treat Achilles tendinitis in a rabbit model of Achilles tendinitis. METHODS: Thirty New Zealand rabbits were randomized into a control group, a model group and an ultrasonic emulsification group. A model of Achilles tendinitis was built in the model and ultrasonic emulsification groups by collagenase injection. Rabbits in the control and model groups were only given normal saline, while those in the ultrasonic emulsification group were subjected to ultrasonic emulsification under guidance of B-mode ultrasonic scan within at 3 weeks after modeling. Three weeks after treatment, tendon repair was estimated by biomechanical analysis, hydroxyproline concentration measurement, and hematoxylin-eosin staining of the tendon tissue. RESULTS AND CONCLUSION: Three weeks after ultrasonic emulsification treatment, hematoxylin-eosin staining showed that the disordered arrangement of collagen fibers and the cell condensation were improved compared with the model group, while the biomechanical analysis and hydroxyproline concentration showed no relief in tendinitis. Therefore, ultrasonic emulsification treatment has an application prospect in tendon repair; however, it is necessary to further explore and optimize the treatment parameters and modes to improve the therapeutic effect in many aspects. Figures and Tables | References | Related Articles | Metrics

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Microglia in spinal cord injury: M1/M2 phenotypic polarization and neurotoxic/neuroprotective effects Li Chuanhong, Yu Xing, Yang Yongdong, Zhao He 2022, 26 (14):  2265-2272.  doi: 10.12307/2022.493 Abstract ( 1058 )   PDF (915KB) ( 53 )   Save BACKGROUND: A large number of studies have shown that microglia are activated after spinal cord injury, which play a dual role of neuroprotection and neurotoxicity, and are closely related to secondary spinal cord injury. OBJECTIVE: To review the characteristics of microglia’ M1/M2 phenotype after spinal cord injury, the progress in spinal cord injury intervention studies targeting M1/M2 phenotype and the possible research directions of microglia after spinal cord injury. METHODS: In May 2021, the first author searched PubMed database with the keywords of “microglia, spinal cord injury, M1 phenotype, M2 phenotype, polarization, activation, activated, regulation.” After reading the title and abstract, the retrieved articles were screened according to the inclusion and exclusion criteria. Finally, a total of 76 included literatures were summarized and reviewed. RESULTS AND CONCLUSION: Microglia have special biological functions due to its unique cell origin and development environment. In physiological state, microglia rely on its highly active branching process to continuously monitor the changes of microenvironment in the spinal cord tissue and play the function of immune surveillance. After spinal cord injury, microglia rapidly respond to abnormal microenvironmental signals and are polarized into M1 and M2 phenotypes, exerting neurotoxic and neuroprotective effects, respectively. A large number of basic experiments have demonstrated that interventions such as Chinese herbal extracts, clinical drugs, regulation of gene expression, cell transplantation, biomaterials can regulate the M1/M2 phenotype of microglia and improve the prognosis of spinal cord injury in a rodent model. However, no consensus has been reached on the optimal regulation target for the quantity and proportion of M1 and M2 phenotypes, and in vivo drug delivery targeting microglia is lacking. Future explorations should focus on promoting the functional balance between M1 and M2 phenotypes to limit the level of inflammatory response after spinal cord injury, which is conducive to repair of the injured spinal cord. With the further research on the precise regulation mechanism of microglial polarization phenotype after spinal cord injury, the results from basic research are correspondingly expected to be applied to clinical treatment. Figures and Tables | References | Related Articles | Metrics

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Advances in animal models of pulmonary fibrosis induced by biotic and abiotic factors Guo Qiqi, Li Yi, Weng Huanze, Wang Qian, Jia Min 2022, 26 (14):  2273-2278.  doi: 10.12307/2022.494 Abstract ( 594 )   PDF (750KB) ( 51 )   Save BACKGROUND: Pulmonary fibrosis is a chronic lung tissue injury with unknown pathogenesis and poor prognosis. At present, the commonly used animal models of pulmonary fibrosis are induced by biological or abiotic factors, which are of great significance to study the pathogenesis, morphological and functional changes and treatment of pulmonary fibrosis. However, most studies have not systematically elucidated the differences between biological and abiotic factors induced pulmonary fibrosis model animals. OBJECTIVE: To review the construction methods of animal models of pulmonary fibrosis so as to provide references for further clinical research and provide design ideas for further improvement of pulmonary fibrosis models in the future. METHODS: Relevant literatures from 1998 to 2021 were retrieved in CNKI, WanFang Data, PubMed, Coremine, SCI-HUB and GeenMedical databases. The keywords used were “pulmonary fibrosis, animal model of pulmonary fibrosis, biological factors, abiotic factors” in Chinese and English, respectively. A total of 51 articles were included for further review and analysis. RESULTS AND CONCLUSION: Animal models of pulmonary fibrosis can be established using biological factors and abiotic factors. Although the pulmonary fibrosis model that is induced by abiotic factors is unstable in the degree of pulmonary fibrosis, it is commonly used because of diverse drugs and routes of administration, easy to operate, and low cost. The methods used for establishing the pulmonary fibrosis model induced by abiotic factors mainly include drug/toxic factors (bleomycin, amiodarone, oleic acid, paraquat, fluorescein isothiocyanate), environmental factors (silica, asbestos, high concentration of oxygen) and other factors (humanization and aging). Pulmonary fibrosis models induced by biological factors are more common induced by cytokine overexpression or targeting type II alveolar epithelial cell damage. This type of model has similar clinical manifestation with pulmonary fibrosis in the late stage, which is stable but expensive. Bleomycin-induced modeling method is more commonly used. This method allows a variety of drug-delivery ways, and has high stability when using nasal feeding. It is safe and less liable to cause accidental death of mice, and has short modeling cycle and low modeling cost. However, the disadvantage of this method is that the induced fibrosis is only the general form of interstitial fibrosis without specificity; and when modeling using environmental factors, the most recommended inducer is silica, but it is now rarely used due to a great damage to the human body. This review considers comprehensively that comparing biological and abiotic factors in the establishment of the animal models of pulmonary fibrosis will help to select the appropriate model in animal experiments; as per the researchers’ own experimental purpose and needs, it is a better choice to induce the pulmonary fibrosis model using bleomycin via nasal feeding. Figures and Tables | References | Related Articles | Metrics

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Effects of SOX9 on chondrocyte differentiation Yang Shuang, Yan Jinglong 2022, 26 (14):  2279-2284.  doi: 10.12307/2022.495 Abstract ( 659 )   PDF (627KB) ( 126 )   Save BACKGROUND: Chondrocytes are the source of seed cells for cartilage repair engineering. Chondrocyte differentiation is closely related to endochondral ossification, which is an essential for bone development. SOX9 plays an important role in the regulation of chondrocytes. OBJECTIVE: To review the latest research progress in the regulatory mechanism of SOX9 on chondrocyte differentiation at different levels. METHODS: A computer search was conducted for the relevant literatures published in CNKI, WanFang, and PubMed until December 2020. The key words were “cartilage, chondrocyte, regulation of SOX9 gene expression, posttranscriptional regulation, protein processing, posttranslational modification, functional partner” in Chinese and “cartilage, chondrocyte, posttranscriptional regulation, posttranslational modification, SOX9, transcriptional regulation, gene expression regulation, SOX9 transcription factor“ in English, respectively. Finally, 61 eligible articles were included for further review. RESULTS AND CONCLUSION: The key mechanisms involved in SOX9 regulation at the gene, RNA, and protein levels have been discovered. The SOX9 key factors can directly or indirectly promote osteogenic growth of chondrocytes, either positively or negatively, or even due to the interaction between various factors. SOX9 is a key factor in chondrocyte differentiation and chondrogenesis. By systematically analyzing the molecular mechanism of SOX9 regulation at different levels, the theoretical basis for cartilage tissue engineering can be provided, to accelerate the clinical treatment and application in cartilage diseases. Figures and Tables | References | Related Articles | Metrics

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Macrophage polarization effectively promotes nerve regeneration after peripheral nerve injury through the M2 phenotypic regulation Hu Taotao, Chang Shusen, Wei Zairong 2022, 26 (14):  2285-2290.  doi: 10.12307/2022.496 Abstract ( 594 )   PDF (638KB) ( 51 )   Save BACKGROUND: Peripheral nerves are the most fragile structure of the human body and are easily damaged by trauma. Macrophages, as the most important immune cells in the peripheral nerves, play an extremely important role in the repair and regeneration of peripheral nerves. As the research on the functions and induction mechanisms of the subtypes of macrophages becomes more and more clear, molecular biology methods can be used to induce macrophages into the corresponding repair phenotype, which is expected to become a new therapeutic target for peripheral nerve injury. OBJECTIVE: To summarize the origin and classification of macrophages in the peripheral nervous system, the polarization of macrophages, the regulation of polarization, and their applications in the repair and regeneration of peripheral nerve injuries. METHODS: CNKI, WanFang, PubMed, and Web of Science were searched for relevant articles using the keywords of “macrophage polarization, nerve” in Chinese and English, respectively. According to the inclusion and exclusion criteria, after initial retrieval, 73 articles with high relevance and reference value were reviewed. RESULTS AND CONCLUSION: Macrophage polarization plays an important role in the repair of peripheral nerve injury, which is expected to become a therapeutic target for the treatment of peripheral nerve injury. However, the mechanism that controls this process still needs to be further studied, and the best method to promote the polarization of macrophage M2 is also uncertain. Therefore, it is necessary to further study the regulation mechanism of macrophages to M2 polarization and how M2 macrophages regulate the recovery of nerve function, and lay the foundation for the treatment of peripheral nerve injury.  Figures and Tables | References | Related Articles | Metrics

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Pathological changes caused by mutations in polydactyly related genes Li Qingman, Guo Feng, Liu Fangfang, Zhang Haiying, Liu Hui 2022, 26 (14):  2291-2296.  doi: 10.12307/2022.497 Abstract ( 684 )   PDF (739KB) ( 120 )   Save BACKGROUND: Congenital polydactyly is the most common limb deformity in clinic, which can be divided into syndromic and non-syndromic types. Non-syndromic type can be further divided into pre-axial polydactyly, post-axial polydactyly, and complex polydactyly, which usually affect the appearance, and even seriously impact the function of fingers(toes). Patients with syndromic polydactyly (toe) deformity have specific clinical manifestations such as developmental delay and mental retardation. OBJECTIVE: To summarize the genes and signal pathways related to the occurrence of polydactyly in order to understand the pathogenesis of polydactyly. METHODS: CNKI, WanFang, VIP, PubMed, and Sci-Hub were retrieved for literatures related to polydactyly published in recent 20 years. The keywords used were “polydactyly, gene, gene mutation, pathway” in English and Chinese, respectively. RESULTS AND CONCLUSION: Existing research on the mechanism of polydactyly has found genes associated with polydactyly, such as GLI3, SHH, TWIST1, LMBR1, FGF, and signaling pathways, such as GLI3-SHH, TGF-beta and Wnt. Therefore, whether there is mutual influence and influence mechanism between signal pathways is one of the directions of future exploration. Although much progress has been made in the research on polydactyly genes, there are still many difficulties to overcome. Figures and Tables | References | Related Articles | Metrics