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18 June 2023, Volume 27 Issue 17 Previous Issue    Next Issue

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Effects of resveratrol on mitochondrial dynamics in rats with exercise-induced fatigue Lou Xujia, Ruan Rong, Jin Qiguan, Hu Yulong 2023, 27 (17):  2625-2630.  doi: 10.12307/2023.192 Abstract ( 299 )   PDF (845KB) ( 94 )   Save BACKGROUND: Resveratrol is a polyphenolic compound found in grapes, peanuts, quinoa and other plants, and act as a kind of health food supplement. Resveratrol supplementation can alleviate exercise fatigue but its specific mechanism is still unclear. This study attempted to investigate its mechanism from the perspective of mitochondrial dynamics. OBJECTIVE: To investigate the effect of resveratrol supplementation on mitochondrial dynamics in a rat model of exercise-induced fatigue. METHODS: Forty-eight Sprague-Dawley male rats were randomly divided into blank control group, resveratrol group, exercise group and exercise+resveratrol group (n=12 per group). The exercise+resveratrol group and the exercise group simultaneously performed a 6-week swimming training with a weight of 5%, 60 minutes once, 6 days per week. The exercise+resveratrol group was given resveratrol 50 mg/kg by gavage 1 hour after exercise and the resveratrol group was only given resveratrol 50 mg/kg by gavage. The blank control and exercise groups were fed with the same volume of solvent every day. Samples were collected at 24 hours after the last exercise. Blood urea nitrogen level, malondialdehyde content, and superoxide dismutase activity in plasma were measured. mRNA expression levels of mitochondrial fusion-related factors (mitochondrial fusion protein 1, mitochondrial fusion protein 2, optical atrophy 1) and fission-related factors (dynamin-related protein 1 and mitochondrial fission protein 1) in the skeletal muscle were determined.  RESULTS AND CONCLUSION: Compared with the blank control group, the levels of blood urea nitrogen and malondialdehyde in the plasma were significantly increased in the exercise group (both P < 0.05), and the superoxide dismutase activity was significantly decreased (P < 0.05). Compared with the exercise group, the levels of urea nitrogen and malondialdehyde in the plasma were significantly decreased in the exercise+resveratrol group (P < 0.01, P < 0.05), and the activity of superoxide dismutase was significantly increased (P < 0.01). Compared with the blank control group, the mRNA expressions of mitochondrial fusion proteins 1 and 2 were significantly decreased in the exercise group (P < 0.01, P < 0.05). Compared with the exercise group, the mRNA expressions of mitochondrial fusion proteins 1 and 2 and optical atrophy 1 were significantly increased in the exercise+resveratrol group (P < 0.01, P < 0.05, P < 0.05). Compared with the blank control group, the mRNA expressions of dynamin-related protein 1 and mitochondrial fission protein 1 were significantly increased in the exercise group (P < 0.01, P < 0.01). Compared with the exercise group, the mRNA expressions of dynamin-related protein 1 and mitochondrial fission protein 1 were significantly decreased in the exercise+resveratrol group (P < 0.01, P < 0.05). These findings indicate that supplementation of resveratrol can promote mitochondrial fusion, inhibit excessive mitochondrial fission, improve mitochondrial dynamics disorder, and accelerate the elimination of exercise-induced fatigue in the rat model of fatigue. Figures and Tables | References | Related Articles | Metrics

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Establishment of an animal model of radioactive 131I-induced hypothyroidism in rats Zhan Ying, Wu Xiaodan, Hao Shanhu 2023, 27 (17):  2631-2636.  doi: 10.12307/2023.195 Abstract ( 272 )   PDF (1145KB) ( 128 )   Save BACKGROUND: Up to now, there is no unified conclusion on the selection of animals and drug doses and the criteria for successful modeling in the modeling process of hypothyroid animal models. OBJECTIVE: To explore the feasibility and optimal dose of radioactive 131I in the establishment of hypothyroidism model in rats METHODS: Forty healthy male Sprague-Dawley rats were randomly divided into five groups (n=8 per group). Four groups were injected intraperitoneally with 4.625, 9.25, 12.95, and 18.5 MBq 131I solution to construct hypothyroidism models and the control group was injected with the same amount of normal saline. The body mass of rats was measured before 131I injection, 4, 8, 12, and 16 weeks after injection of 131I. The serum levels of thyroid-stimulating hormone, free triiodothyronine, free thyroxine, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, blood urea nitrogen, creatinine, and uric acid were determined by an ELISA kit. Thyroid function was evaluated by 131I static imaging and morphological changes of thyroid tissue were observed by hematoxylin-eosin staining. RESULTS AND CONCLUSION: Compared with the control group, the body mass of the rats in the 9.25, 12.95, and 18.5 MBq groups were significantly decreased at 8, 12, and 16 weeks (P < 0.05). The serum thyroid-stimulating hormone concentration gradually increased in the 9.25, 12.95, and 18.5 MBq groups at 4, 8, 12, and 16 weeks, while the levels of free triiodothyronine and free thyroxine gradually decreased (P < 0.05). The levels of alanine aminotransferase and alkaline phosphatase in the 12.95 and 18.5 MBq groups were significantly higher than those in the control group, while the blood urea nitrogen and creatinine levels in the 18.5 MBq group were significantly higher than those in the control group (P < 0.05). The thyroid glands in each group were clearly visualized before 131I injection, and the target-to-nontarget ratio was not significantly different among groups (P > 0.05). Compared with the control group, the thyroid glands of the 9.25, 12.95, and 18.5 MBq groups were not visualized in the 4th week and the target-to-nontarget ratio was significantly decreased (P < 0.05). The thyroid glands were undeveloped at the 8-, 12-, and 16-week follow-up visits, but there was no statistical difference in the target-to-nontarget ratio among groups (P > 0.05). After injection of 131I, the thyroid follicles of rats became smaller and shrunken, and some of them were irregular. All these findings indicate that intraperitoneal injection of 131I at a dose of 9.25 MBq could successfully establish a stable hypothyroid model in rats within 4 weeks, which provide a reference for the establishment of animal models in the field of nuclear medicine 131I therapy. Figures and Tables | References | Related Articles | Metrics

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Bioinformatic analysis and experimental validation of ferroptosis in osteoarthritis Li Zhe, Yuan Changshen, Guan Yanbing, Xu Wenfei, Liao Shuning, Rong Weiming, Mei Qijie, Duan Kan 2023, 27 (17):  2637-2643.  doi: 10.12307/2023.437 Abstract ( 425 )   PDF (1492KB) ( 48 )   Save BACKGROUND: Regulating ferroptosis by targeting iron overload genes may be a fast and effective way to delay the degeneration of osteoarthritis. However, the molecular mechanisms and gene targets related to ferroptosis in osteoarthritis are still unclear. OBJECTIVE: To analyze the key genes and pathways of ferroptosis in osteoarthritis by bioinformatics analysis, verify the marker genes of ferroptosis in combination with in vitro experiments, and explore the potential role of ferroptosis in osteoarthritis. METHODS: “Osteoarthritis” was used as a keyword. Relevant public data from the GEO database between January 1, 2010 and January 1, 2021 were retrieved. A gene microarray dataset GSE55235 was yielded and differentially expressed genes were identified after data correction analysis of the GSE55235 data set. Ferroptosis-related genes retrieved by the FerrDb database were intersected with differentially expressed genes in the GSE55235 dataset, and th intersected genes were used for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis and the protein-protein interaction network was mapped. Ferroptosis-related HUB genes in osteoarthritis were obtained and ferroptosis marker genes were then selected. Human chondrocytes were divided into control group (normal human chondrocytes) and experimental group (cellular osteoarthritic model). The mRNA expression of ferroptosis marker genes in the two groups was detected by quantitative real-time fluorescence PCR. RESULTS AND CONCLUSION: A total of 36 ferroptosis-related genes in osteoarthritis were obtained. Gene Ontology enrichment analysis showed that these differentially expressed genes were mainly involved in oxidative stress, corticosteroids response, steroid hormone response, glucocorticoid response, and reactive oxygen metabolism, and play a role in NAD(P)H oxidase and oxidoreductase activity, heme binding, and tetrapyrrole binding that produce superoxides. Kyoto Encyclopedia of Genes and Genomes enrichment analysis showed that ferroptosis-related genes in osteoarthritis were mainly involved in NOD-like receptor, interleukin-17, hypoxia-inducible factor-1, tumor necrosis factor, forkhead box transcription factor class O. After constructing the protein-protein interaction network, ferroptosis-related HUB genes, including vascular endothelial growth factor A, interleukin-6, JUN, PTGS2, DUSP1, were identified. Four ferroptosis marker genes, including vascular endothelial growth factor A, interleukin-6, PTGS2, and DUSP1, were selected. In vitro experiments confirmed significant differences between the control and experimental groups (P < 0.05). The overall findings indicate that ferroptosis may act on osteoarthritis through oxidative stress, redox and induced inflammation, which may be related to NAD(P) H stimulation by signaling pathway such as hypoxia-inducible factor 1. Vascular endothelial growth factor A, interleukin-6, PTGS2, and DUSP1 can be used as biomarkers of ferroptosis in osteoarthritis. Figures and Tables | References | Related Articles | Metrics

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Pathological changes and expression of related adhesion molecules in vascular endothelial cell injury in heatstroke pigs Hu Lingling, Ni Jun, Fu Gang, Zhang Jing 2023, 27 (17):  2644-2650.  doi: 10.12307/2023.146 Abstract ( 291 )   PDF (1927KB) ( 130 )   Save BACKGROUND: Heatstroke is a highly fatal syndrome characterized by extensive endothelial cell injury and multiple organ failure caused by high temperature. The common complication is abnormal coagulation function, and vascular endothelial disease plays a key role in the coagulation disorder caused by severe heatstroke. OBJECTIVE: To observe the pathological changes of vascular endothelial cell injury in severe heatstroke pigs and the expression of intercellular cell adhesion molecule-1. METHODS: Twelve healthy male Bama miniature pigs (conventional animals) weighing 15-20 kg were randomly divided into normal temperature control group (n=6) and heatstroke group (n=6). Severe heatstroke pig model was made in the heatstroke group under high temperature and humidity environment. The pigs in the normal temperature control group were placed in a constant temperature humidity chamber. Venous blood samples before and after the experiment was collected for blood routine and coagulation function examinations in the two groups. The abdominal aorta, coronary artery and lung tissue samples at the same position were taken, and the pathological changes of the samples in the two groups were observed by hematoxylin-eosin staining. Immunohistochemical staining was used to observe the level of intercellular adhesion molecule-1 in the two groups. The ultrastructural changes of the coronary artery and lung were observed by high-power transmission electron microscope. RESULTS AND CONCLUSION: There were no significant changes in activated partial thromboplastin time, prothrombin time, plasma D-dimer, fibrinogen degradation product level and red blood cell and platelet counts in the normal temperature control group before and after the experiment (P > 0.05). The red blood cell count, activated partial thromboplastin time, prothrombin time, plasma D-dimer and fibrinogen degradation products in the heatstroke group increased significantly after the experiment and were higher than those in the normal temperature control group. Whereas, the platelet count decreased in the heatstroke group after the experimental and was significantly lower than that in the normal temperature control group (P < 0.05). Hematoxylin-eosin staining revealed that the pathological structure of abdominal aorta, coronary artery and pulmonary microvessels in the normal temperature control group was normal. Abdominal aortic endothelial cells in the heatstroke group were slightly edematous without obvious abnormalities; thrombosis, endothelial cell abscission, and necrosis were observed in the coronary artery, and the cell number decreased; and pulmonary microvascular diffuse hemorrhage and the number of endothelial cells decreased significantly. Immunohistochemical staining showed that the positive expression of intercellular adhesion molecule-1 with a large number of brownish yellow lines on the serosa of endothelial cells was observed in the abdominal aorta, coronary artery and lung of normal temperature control group; the number of endothelial cells on the serosa decreased significantly or the expression was absent and the light yellow intercellular adhesion molecule-1 was weakly positive in the heatstroke group; the average absorbance value of intercellular adhesion molecule-1 in vascular tissue in the heatstroke group was significantly lower than that in the normal temperature control group (P < 0.05). Under the electron microscope, irregular nuclei and swollen mitochondria were observed in coronary artery tissue in the heatstroke group, as well as a small amount of swollen nuclei and mitochondria observed in the lung tissue. To conclude, heatstroke can cause an injury to vascular endothelial cells, especially microvascular injury, in miniature pigs. Figures and Tables | References | Related Articles | Metrics

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Effects of mitochondrial fission inhibitor-1 on neurotrophic factor and neural inhibitory signaling pathway in a mouse model of multiple sclerosis Zhang Wei, Liu Ziming, Zhang Nianping, Tian Sixie, Zhang Siyu, Li Yanhua, Ma Cungen 2023, 27 (17):  2651-2657.  doi: 10.12307/2023.474 Abstract ( 306 )   PDF (3139KB) ( 104 )   Save BACKGROUND: Decreased expression of neurotrophic factors and increased expression of regenerating inhibitors are the main mechanisms of nerve injury. It has been proven that mitochondrial fission inhibitor-1 can decrease clinical score and relieve pathological injury in a mouse model of multiple sclerosis. However, its neuroprotective effects still need to be further explored. OBJECTIVE: To observe the state of neurons and axons in a mouse model of experimental autoimmune encephalomyelitis and to evaluate the neuroprotective effect of mitochondrial fission inhibitor-1. METHODS: A mouse model of experimental autoimmune encephalomyelitis was prepared in C57BL/6 mice by immunizing with myelin oligodendrocyte glycoprotein peptide fragment 35-55. Animal models were randomly divided into two groups (n=15 per group): model group and mitochondrial fission inhibitor-1 group. Mice were euthanized and lumbar spinal cord consecutive sections were harvested at day 28 post immunization. Immunofluorescence staining was used to analyze the state of neuronal cell body and synapse, the phosphorylation level of dynamin-related protein 1, and the expression of neurotrophic factor, regeneration inhibitor and its signaling pathway molecules in spinal cord tissue. RESULTS AND CONCLUSION: Compared with the model group, treatment with mitochondrial fission inhibitor-1 increased the number of neurons marked by neuron-specific nuclear protein in the spinal cord tissue, improved neuronal body morphology, increased the length of synaptophysin-positive synapse, decreased the loss of Neurofilament M, and inhibited the phosphorylation of dynamin-related protein 1. Mitochondrial fission inhibitor-1 treatment could significantly promote the expression of glial cell-derived neurotrophic factor, ciliary neurotrophic factor, and brain-derived neurotrophic factor. Mitochondrial fission inhibitor-1 intervention could markedly reduce the expression of myelin-associated glycoprotein, axon growth inhibitory factor A, axon growth inhibitory factor protein receptor, p75 neurotrophin protein receptor, and Rho-related protein kinase II in the mouse model. To conclude, mitochondrial fission inhibitor-1 can inhibit the phosphorylation level of dynamin-related protein 1, increase the expression of neurotrophic factor protein, and reduce the expression of regeneration inhibitor and related signaling pathway molecular proteins, thus alleviating damage to spinal cord neuron cell bodies, axons, and cysts. Figures and Tables | References | Related Articles | Metrics

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Effects of mecobalamin on neuropathic pain and acid-sensing ion channels in a rat model of lumbar disc herniation Wang Chunyu, Chen Zhigang, Zhang Jianli 2023, 27 (17):  2658-2663.  doi: 10.12307/2023.191 Abstract ( 370 )   PDF (1113KB) ( 95 )   Save BACKGROUND: Acid-sensing ion channels can be involved in various physiological processes, such as synaptic plasticity, pain perception, and touch. Inflammation can trigger the activation and change of acidic microenvironment, which may be an important factor leading to persistence and high recurrence rate of related diseases. OBJECTIVE: To investigate the effects of mecobalamin on neuropathic pain, c-Jun N-terminal kinase and chemokine (C-X-C motif) ligand 1 pathways and acid-sensing ion channels in rats with lumbar disc herniation. METHODS: Forty healthy Sprague-Dawley rats were randomized into control group, model group, mecobalamin group, and drug control group (n=10 per group). The lumbar disc herniation model was established in the rats except for the control group. The model and groups were intraperitoneally injected with 0.8 mL/kg/d normal saline. The mecobalamin group was intraperitoneally injected with 104 μg/kg/d. The drug control group was intraperitoneally injected with celecoxib 0.5 mL/kg/d. Administration in each group was performed once a day for 14 days. Mechanical paw withdrawal thresholds were measured with an intelligent hot plate instrument 1 day before modeling, 1 day after modeling, and 7 and 14 days after treatment. PCR was used to detect the mRNA expression of acid-sensing ion channels 24 hours after administration. The levels of inflammatory factors, interleukin-6 and tumor necrosis factor α, were detected by ELISA at 7 and 14 days after treatment. Western blot assay was used to detect c-Jun N-terminal kinase and chemokine (C-X-C motif) ligand 1 protein levels. RESULTS AND CONCLUSION: Compared with the control group, the mechanical paw withdrawal threshold of the hind limbs was significantly decreased in the model group (P < 0.05). The mechanical paw withdrawal threshold of the hind limbs was significantly higher in the mecobalamin group than the model group  (P < 0.05) and the drug control group (P < 0.05). Compared with the control group, the levels of interleukin-6 and tumor necrosis factor α were increased in the model group (P < 0.05). While compared with the model and drug control groups, mecobalamin could significantly reduce the levels of interleukin-6 and tumor necrosis factor α (both P < 0.05). In the model group, neurons were vacuolated and irregular, with blurred and disordered nucleoli; in the mecobalamin group, a small number of neurons were pyknotic and presented with nuclear migration, the voiding area in the gray and white matter was reduced, the nucleoli were clear, and Nissl bodies in the cytoplasm were relatively uniform; in the drug control group, some neurons still presented with pyknosis, necrosis, and dissolution and the voiding area in the gray and white matter was reduced. Compared with the control group, the mRNA levels of acid-sensing ion channels 3 and 1a in the spinal dorsal horn of rats were significantly increased (P < 0.05) and the protein expressions of c-Jun N-terminal kinase and chemokine (C-X-C motif) ligand 1 were significantly upregulated in the model group (P < 0.05). The levels of the above-mentioned indicators were significantly lower in the mecobalamin group than the model and drug control groups (P < 0.05). To conclude, mecobalamin can alleviate neuropathic pain and inhibit the expression of inflammatory factors in serum and the activity of acid-sensing ion channels in rats with lumbar disc herniation. The mechanism may be related to the inhibition of c-Jun N-terminal kinase and chemokine (C-X-C motif) ligand 1 expression. Figures and Tables | References | Related Articles | Metrics

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Comparative study of traumatic heterotopic ossification in mice induced by Achilles tenotomy combined with skin burn injury and single Achilles tenotomy Wang Zheng, Chen Hongshu, Yi Xinzeyu, Li Zonghuan 2023, 27 (17):  2664-2668.  doi: 10.12307/2023.432 Abstract ( 301 )   PDF (1166KB) ( 132 )   Save BACKGROUND: At present, Achilles tenotomy model is an animal model mainly used for traumatic heterotopic ossification. However, this method requires a long time to form ectopic bone, and the size of the formed ectopic bone is always small. In addition, this method cannot accurately reproduce the systemic inflammatory state of most traumatic heterotopic ossification cases in clinic practice. OBJECTIVE: To verify the validity of the animal model of traumatic heterotopic ossification induced by Achilles tenotomy combined with skin burn injury, to compare this approach with single Achilles tenotomy, and to evaluate the practicability of the two methods.  METHODS: Forty male C57BL/6 mice were randomly divided into two groups: Achilles tenotomy group (control group, n=20) and Achilles tenotomy+30% skin scald on the back group (experimental group, n=20). The survival rate and healing of surgical incisions of the mice in the two groups were recorded. Survival rate and wound healing in the two groups as well as skin recovery of burn injury in the experimental group were recorded. Micro-CT examination and Masson staining of the Achilles tendon was performed 8 weeks after surgery to observe the ectopic bone at the surgical site. Formation of ectopic bone was also observed in the two groups.  RESULTS AND CONCLUSION: There was no death and wound infection in the two groups. The skin burn injury in the experimental group recovered well without ulceration. Micro-CT findings indicated that all mice in the experimental group developed traumatic heterotopic ossification, with obvious circular high-density shadow at the surgical site, and the volume of ectopic bone was (2.72±0.04) mm3. In contrast, only 17 mice developed traumatic heterotopic ossification in the control group, and the volume of ectopic bone was (0.65±0.08) mm3. There was a significant difference in the volume of ectopic bone between the two groups (P < 0.05). Masson staining showed that ectopic bone in both groups had bone trabecular and bone marrow structures, but the area of ectopic bone in the experimental group was significantly larger than that in the control group (P < 0.05). To conclude, Achilles tenotomy combined with skin burn injury can effectively induce traumatic heterotopic ossification earlier than single Achilles tenotomy in mice. This combination method has a higher successful rate and can produce larger size of ectopic bone, which can be an ideal method to establish an animal model of traumatic heterotopic ossification. Figures and Tables | References | Related Articles | Metrics

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Oligodendrocyte progenitor cells prolong the survival of glioblastoma-bearing rats after high-dose radiotherapy Gao Yue, Lin Jianwen, Li Di, Lan Xiaoyan, Li Shen, Chu Chengyan 2023, 27 (17):  2669-2674.  doi: 10.12307/2023.186 Abstract ( 295 )   PDF (1516KB) ( 88 )   Save BACKGROUND: Glioblastoma is a common malignant brain tumor for adults with poor prognosis and remains lack of efficient treatments.  OBJECTIVE: To investigate the efficacy of single high-dose radiotherapy on glioblastoma and the feasibility of oligodendrocyte progenitor cells in the repair of radiation-induced brain injury. METHODS: Plasmid transfection was used to develop human U-87 MG cell line expressing luciferase (Luc). Fifteen Fisher 344 rats bearing Luc-U-87 MG glioblastoma were randomly divided into tumor model group (n=3), radiotherapy group (n=6), and oligodendrocyte progenitor cell transplantation group (n=6). Single high-dose radiotherapy (80 Gy) was given in the latter two groups and cell transplantation was performed in the last group 5 weeks after radiotherapy. In vivo imaging was employed to monitor the tumor growth. MRI was performed to observe the cerebral structure changes induced by radiation. Kaplan-Meier analysis was used to determine the effect of cell transplantation on the survival rate of irradiated rats. Survival and differentiation of transplanted cells were histologically observed.  RESULTS AND CONCLUSION: In vitro imaging results showed that the transfected U-87 MG cells reacted with the Luc substrate to produce bioluminescence signals. Signal intensity had a positive linear correlation with the number of transfected cells. Intracranial glioblastoma signals in the tumor model rats continued to increase until their death at 5 weeks after tumor inoculation. Two weeks after radiotherapy, the bioluminescence signal started to decline in the radiotherapy group and was not detected at 4 weeks. Necrotic tumor tissue was observed on T2WI at 5 weeks after radiotherapy but not at 10 weeks, at which timepoint the abnormal signal indicative of brain injury appeared. However, there were no similar signals in the cell transplantation group. Fifteen weeks later, T2WI showed hypo- and hyperintensity signals in the brain parenchyma for all the rats which received irradiation, whereas the injury signal in the radiotherapy group was stronger than that in the cell transplantation group. The survival analysis results revealed the median survival time of the tumor model group, radiotherapy group, and cell transplantation group were 30, 114.5, and 232.5 days, respectively. There were significant differences in the median survival time among groups (P < 0.01). Histological findings showed the transplanted cells survived with multipolarity and some of them expressed myelin basic protein. Moreover, the expression of myelin basic protein in the cell transplantation group was significantly higher than that in the radiotherapy group (P < 0.01). All these findings indicate that single high-dose radiotherapy can effective treat human-derived glioblastoma in rats. Oligodendrocyte progenitor cells transplanted are capable of repairing radiation-induced brain injury, thereby prolonging the survival of irradiated rats. Remyelination is one of the mechanisms accounting for brain tissue repair.   Figures and Tables | References | Related Articles | Metrics

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Correlation between femur bone morphogenetic protein 2 expression and bone fluoride content in fluorosis rabbits Liang Weiye, Duan Qinghong 2023, 27 (17):  2675-2680.  doi: 10.12307/2023.158 Abstract ( 233 )   PDF (1103KB) ( 137 )   Save BACKGROUND: Fluorosis is a common endemic disease, and its severity depends on the dose and duration of fluoride exposure. Bone morphogenetic protein 2 plays an important role in the pathogenesis of skeletal fluorosis. OBJECTIVE: To explore the relationship between the expression of bone morphogenetic protein 2 and bone fluoride content in rabbit femur and the changes of bone formation markers, osteocalcin and procollagen l N-terminal propeptide, under different fluoride concentrations.   METHODS: Sixteen New Zealand white rabbits were randomly divided into control group, low dose group, middle dose group, and high dose group, with four rabbits in each group. Animals drank tap water containing 0, 100, 200, and 400 mg/L sodium fluoride, respectively. The experimental period was 6 months. During the feeding period, all animals had free access to water and food. Occurrence and development of dental fluorosis was observed regularly. The fluorine content in rabbit femur was determined by ashing distillation-fluorine reagent colorimetry. The expression of bone morphogenetic protein 2 in femur was detected by western blot. The levels of osteocalcin and procollagen l N-terminal propeptide in serum were detected by enzyme-linked immunosorbent assay.   RESULTS AND CONCLUSION: The rabbits in fluoride exposure groups showed different degrees of fluorosis. In the low dose group, mild fluorosis was found and mainly manifested with tarnished teeth and some fine lines. The middle dose group was dominated by moderate dental fluorosis, manifested as uneven tooth surface and color. Some models with dental defects presented with severe dental fluorosis. The high dose group was dominated by severe dental fluorosis, which was characterized by dull tooth surface and deformed tooth development. The bone fluoride content in the femur of rabbits increased with the increase of fluoride intake, which was higher in the high dose group than the other three groups (P < 0.01, P < 0.001). The serum osteocalcin level in the high dose was higher than that in the control group (P < 0.05) and the serum level of procollagen l N-terminal propeptide was lower than that in the control group and the low dose group (P < 0.05). The expression of bone morphogenetic protein 2 in the femur was higher in the low dose group than the control and high dose groups (P < 0.05). Pearson correlation analysis showed that the expression of bone morphogenetic protein 2 in the low dose group was positively correlated with the bone fluoride content (r=0.951, P < 0.05), while there was no significant correlation between the expression of bone morphogenetic protein 2 and the content of bone fluoride in the middle and high dose groups (r=0.889, r=-0.116, P > 0.05). To conclude, the expression of bone morphogenetic protein 2 in rabbit femur is bidirectionally related to bone fluoride concent, which is related to fluoride exposure concentration, that is, too high or too low fluoride content will alter the expression of bone morphogenetic protein 2. Figures and Tables | Related Articles | Metrics

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Ferroptosis is involved in the pathogenesis of liver injury induced by high methionine diet in ApoE-/- mice Li Yuanyuan, Sun Yue, Bao Rui, Chang Sirong, Wang Meng, Yu Mengxue, Yang Anning, Liu Zhihong 2023, 27 (17):  2681-2686.  doi: 10.12307/2023.423 Abstract ( 337 )   PDF (1171KB) ( 96 )   Save BACKGROUND: Homocysteine can promote the occurrence of liver injury through oxidative stress, inflammatory response, and endoplasmic reticulum stress. High methionine diet-induced apolipoprotein gene knockout (ApoE-/-) can induce liver injury and increase in vivo homocysteine level in mice. Ferroptosis is a cellular regulatory death pathway that depends on intracellular iron and causes excessive accumulation of lipid peroxides. However, whether it is involved in the formation of liver injury induced by high methionine diet needs to be further studied and discussed. OBJECTIVE: To explore the role of ferroptosis in hyperhomocysteine-induced liver injury in ApoE-/- mice.  METHODS: Twelve ApoE-/- mice aged 6 to 8 weeks were randomly divided into control group and high methionine group (n=6 per group), and fed with normal diet and high methionine diet for 13.5 weeks. Liver injury in ApoE-/- mice was evaluated by pathological observation and detection of aspartate aminotransferase and alanine aminotransferase activity in liver tissue. Iron ion concentration in liver tissue of mice was tested by tissue iron detection kit. Malondialdehyde content and fluorescence intensity were detected to evaluate the degree of lipid peroxidation in the liver tissue of mice. Real-time fluorescence quantitative PCR and western blot were performed to determine the expression of P53 and glutathione peroxidase 4 at mRNA and protein levels in the liver tissue.  RESULTS AND CONCLUSION: Compared with the control group, a large number of liver cells in the high methionine diet group were found to have the typical histopathological changes of liver injury, such as disordered arrangement of liver cells, enlarged space, and loose cytoplasm. Compared with the control group, the activities of aspartate aminotransferase and alanine aminotransferase were significantly increased (P < 0.01). Meanwhile, the concentration of iron ions (P < 0.01), malondialdehyde content (P < 0.01), and fluorescence intensity in liver tissue were also significantly increased in the high methionine diet group. Real-time fluorescence quantitative PCR and western blot results showed that the expression level of glutathione peroxidase 4 was decreased (P < 0.01) and the expression of P53 was increased (P < 0.05) in ApoE-/- mice in the high methionine diet group. These findings indicate that ferroptosis is involved in the pathogenesis of liver injury in ApoE-/- mice induced by high methionine diet. Figures and Tables | References | Related Articles | Metrics

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Limited-incision knotless repair for acute closed Achilles tendon ruptures Zhou Weibo, Zhang Yi, Liang Wenwei, Zhu Chunhui, Zhou Fulin 2023, 27 (17):  2687-2691.  doi: 10.12307/2023.199 Abstract ( 300 )   PDF (891KB) ( 44 )   Save BACKGROUND: Achilles tendon rupture is a common orthopedic disease in clinical practice. The traditional surgical method results in a large incision and has the high probability of complications. Exploring a minimally invasive surgical treatment is helpful to enhance patient rapid recovery. OBJECTIVE: To investigate the clinical efficacy and feasibility of limited-incision knotless bridging in the treatment of acute closed Achilles tendon rupture.  METHODS: The clinical data of 22 patients with acute closed Achilles tendon rupture treated in Changzhou Second People’s Hospital Affiliated to Nanjing Medical University from January 2019 to May 2020 were retrospectively analyzed. All patients were treated with limited-incision knotless bridging surgery and were followed up for over 12 months. The amount of intraoperative bleeding, operation time, and hospital stay were recorded. The American Orthopaedic Foot & Ankle Society score for ankle-hindfoot function, visual analog scale score, Fugl-Meyer Rating Scale score for the lower limbs and Achilles tendon complete rupture score were compared before operation and at the last follow-up. The complications during follow-up and the curative effect at the last follow-up were analyzed as per the Amer Lindholm evaluation standard. RESULTS AND CONCLUSION: All patients were followed up without incision complications. As per the Amer Lindholm evaluation standard, excellent was in 18 cases (82%) and good in 4 cases (18%). The excellent and good rate was 100%. At the last follow-up, the American Orthopaedic Foot & Ankle Society score, the Fugl-Meyer Rating Scale score for the lower limbs, and Achilles tendon complete rupture score were significantly higher than those before operation, and the visual analogy score was significantly lower than that before operation (P < 0.05). At the last follow-up, there was no significant difference between the affected and health sides in terms of the American Orthopaedic Foot & Ankle Society score for ankle-hindfoot function, visual analog scale score, Fugl-Meyer Rating Scale score for the lower limbs, and Achilles tendon complete rupture score (P > 0.05). To conclude, the limited-incision knotless bridging technique in the treatment of acute Achilles tendon rupture has the advantages of simple operation, less postoperative complications and satisfactory functional recovery. Figures and Tables | References | Related Articles | Metrics

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Acupuncture and moxibustion combined with rehabilitation therapy improve neurological function and intestinal flora following cerebral ischemia in rats Cui Zhenhua, Lin Xiafei, Chen Yongmin, Lin Ye, Li Guanyu, Song Zhenhua 2023, 27 (17):  2692-2698.  doi: 10.12307/2023.157 Abstract ( 265 )   PDF (942KB) ( 98 )   Save BACKGROUND: Both acupuncture and moxibustion and rehabilitation training can effectively alleviate the symptoms of patients with cerebral ischemia. At present, it is unclear whether the combined treatment of the two has a regulatory effect on neurological dysfunction and intestinal flora imbalance in patients with cerebral ischemia and its role mechanism.  OBJECTIVE: To explore the effect of acupuncture and moxibustion combined with rehabilitation therapy on neurological function and intestinal flora in rats with cerebral ischemia.  METHODS: Sixty Sprague-Dawley rats were randomly divided into sham operation group, model group, acupuncture group, rehabilitation group, and acupuncture+rehabilitation group (n=12 per group). Animal models of cerebral ischemia were prepared in all groups except for the sham operation group. In the sham operation group, the left common carotid artery was only separated but not ligated. The acupuncture group was treated with scalp cluster acupuncture intervention, the rehabilitation group was given task-oriented treadmill training, and the acupuncture+rehabilitation group was given scalp cluster acupuncture and task-oriented treadmill training intervention. Treatments in each group lasted for 14 days. The sham operation and model groups were not intervened. The neurological function was assessed by Longa score at 4 hours, 1, 7, and 14 days after modeling. Changes in brain water content were detected after 14 days of intervention. Western blot was applied to detect the expressions of neuron growth-related proteins (growth-associated protein 43, neurofilament 200, repulsive guidance molecule a) in the ischemic penumbra. Kit detection was used for detecting the levels of lactate dehydrogenase, superoxide dismutase, and malondialdehyde in brain tissue. ELISA was applied to detect the levels of tumor necrosis factor-α and interleukin-1β in brain tissue. Real-time fluorescent quantitative PCR was used to detect the changes of Escherichia coli, Bifidobacterium, Lactobacillus, and Enterococcus in rat feces.  RESULTS AND CONCLUSION: At 4 hours, 1, 7, and 14 days after modeling, there was no neurological dysfunction in the sham operation group but obvious neurological dysfunction in the model group (P < 0.05). Compared with the model group, the neurological deficits of rats in the acupuncture and rehabilitation groups were significantly improved with the prolonged intervention time (P < 0.05), and the neurological function of rats in the acupuncture+rehabilitation group improved more significantly (P < 0.01). Compared with the model group, the expressions of growth-associated protein 43 and neurofilament 200 in the ischemic penumbra were significantly up-regulated in the acupuncture and rehabilitation groups (P < 0.05), the expression of repulsive guidance molecule a was significantly down-regulated (P < 0.05), the brain water content and levels of lactate dehydrogenase, malondialdehyde, tumor necrosis factor-α and interleukin-1β in brain tissue were reduced (P < 0.01), the superoxide dismutase level was raised (P < 0.01), the counts of Escherichia coli and Enterococcus in feces were significantly increased (P < 0.01), and the counts of Bifidobacterium and Lactobacillus were significantly decreased (P < 0.01). The above-mentioned indicators were improved more significantly in the acupuncture+rehabilitation group (P < 0.01). To conclude, acupuncture and moxibustion combined with rehabilitation therapy can improve neurological function, relieve oxidative stress and inflammatory responses, and regulate intestinal flora disorders in rats with cerebral ischemia by stimulating the regeneration of neurons in the ischemic penumbra. The combine therapy has a protective effect against ischemic stroke. Figures and Tables | References | Related Articles | Metrics

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Macrophage polarization and periodontitis Yuan Shuyue, Liu Chunyan, Liu Bing, Zhao Fei 2023, 27 (17):  2699-2707.  doi: 10.12307/2023.477 Abstract ( 658 )   PDF (943KB) ( 81 )   Save BACKGROUND: Periodontitis is an inflammation of the periodontal support tissue, manifested as inflammation of the gums and resorption of alveolar bone. Macrophages can play a role in the occurrence and development of periodontitis through M1 and M2 polarization. OBJECTIVE: To review the relationship between macrophage polarization and periodontitis and its related mechanism, so as to provide ideas for the clinical treatment of periodontitis.     METHODS: The first author searched the relevant papers published from 1991 to 2022 in PubMed and CNKI. The search terms in Chinese and English were “macrophage polarization, M1/M2 macrophages, periodontitis.” Preliminary screening was performed by reading the title and abstract. Finally, 97 articles were included and analyzed. RESULTS AND CONCLUSION: As human innate immune cells, macrophages play an important role in the occurrence and development of inflammation. Macrophages can be polarized under environmental stimulation, which is a complex process. Signaling pathways such as JAK/STAT, TLRs/nuclear factor-κB, PI3K/Akt, inflammatory factors such as tumor necrosis factor-α, interferon-γ, interleukin-4, interleukin-13, and epigenetic mechanisms can all influence macrophage polarization. M1-type polarization of macrophages promotes inflammatory progression and M2-type polarization of macrophages exerts anti-inflammatory effects. Studies have found that different polarized types of macrophages play a pro-inflammatory or anti-inflammatory role in the process of periodontitis through various signaling pathways and secretion of inflammatory factors, and influence bone resorption and bone formation through a variety of ways, and then affect the progression of periodontitis. That is, macrophages are polarized through relevant mechanisms and the polarized macrophages can play an anti-inflammatory or pro-inflammatory role in the process of periodontitis, which has an impact on the progression of periodontitis. Therefore, it is of great significance for the treatment of periodontitis to study the role and mechanism of macrophage polarization in the pathogenesis of periodontitis. However, the polarization mechanism of macrophages is not completely clear yet. Therefore, it is of great significance for future treatment of periodontitis to discover the potential mechanism of polarization and combine it with the treatment of periodontitis to promote the transformation of macrophages to M2-type and its proportion or inhibit or reduce the expression of M1-type macrophages in the process of periodontitis. The combination of epigenetics with macrophage polarization and periodontitis at the gene and protein levels may be an effective treatment for periodontitis.   Figures and Tables | References | Related Articles | Metrics

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The regulatory role of Hippo-YAP signaling pathway in exercise-induced cardiac hypertrophy Fan Qinghua, Qi Jie, Zhang Jun 2023, 27 (17):  2708-2715.  doi: 10.12307/2023.443 Abstract ( 294 )   PDF (986KB) ( 89 )   Save BACKGROUND: The Hippo-YAP signaling pathway is a signaling cascade that is highly conserved across species and has attracted widespread attention in the study of physiological cardiac hypertrophy. Studies have found that many pathways such as mechanical force, autophagy, and energy metabolism are involved in the regulation of exercise-induced cardiac hypertrophy. These pathways may interact with the Hippo-YAP signaling pathway after exercise, thereby affecting the formation and development of exercise-induced cardiac hypertrophy.  OBJECTIVE: To summarize the effects of exercise on Hippo-YAP signaling pathway, and describe the potential mechanism of Hippo-YAP signaling pathway in regulating exercise-induced cardiac hypertrophy.  METHODS: “Hippo-YAP signaling pathway, YAP/TAZ, exercise-induced cardiac hypertrophy, heart, exercise” were used as keywords in Chinese and English. Relevant literatures included in CNKI, PubMed, and Web of Science databases from 1983 to 2022 were retrieved, and 70 articles that met the screening criteria were reviewed.   RESULTS AND CONCLUSION: Hippo-YAP signaling pathway is affected by exercise and has a certain regulatory role in exercise-induced physiological cardiac hypertrophy. (1) Hippo-YAP signaling pathway induces mechanical stimulation triggered by exercise, which leads to changes in the activity and expression of YAP/TAZ, and mediates the response of cardiomyocytes to mechanical signals. (2) Hippo-YAP signaling pathway regulates autophagy in cardiomyocytes and maintains the homeostasis, normal structures and physiological functions of cardiomyocytes during exercise. (3) Hippo-YAP signaling pathway may mediate the oxidation and glycolysis of energy substances during exercise-induced cardiac hypertrophy, and may also be affected by energy changes during exercise. (4) Hippo-YAP signaling pathway may strengthen the connection with some non-coding RNAs related to physiological cardiac hypertrophy under the action of exercise, and multiple non-coding RNAs may jointly regulate Hippo-YAP signaling. (5) Hippo-YAP signaling pathway interacts with the classic pathways of exercise-induced cardiac hypertrophy. Exercise promotes the signaling interaction between them and participates in the regulation of exercise-induced cardiac hypertrophy. (6) To deeply study the regulatory role of Hippo-YAP signaling pathway in exercise-induced cardiac hypertrophy will help deepen the understanding of exercise-promoting heart health, and provide new ideas and strategies for the clinical prevention and treatment of cardiac diseases and myocardial tissue construction.  Figures and Tables | References | Related Articles | Metrics

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Piezo1-mediated mechanical stress stimulation in anti-osteoporosis treatment Huang Haoran, Wei Yangwenxiang, Zhang Jiahao, Mo Liang, Liu Yuhao, Chen Zhenqiu, Wang Haibin, Zhou Chi 2023, 27 (17):  2716-2722.  doi: 10.12307/2023.404 Abstract ( 341 )   PDF (1076KB) ( 247 )   Save BACKGROUND: Piezo1 is a mechanosensitive channel that acts as an important target protein for mechanical stress stimulation. Piezo1 converts external mechanical forces into biological signals, regulating bone formation and bone resorption. Piezo1 plays an important role in anti-osteoporosis. OBJECTIVE: To summarize the mechanism of mechanical stress stimulation in anti-osteoporosis and research progress in Piezo1 molecular biology as well as the use of Piezo1 in the treatment of osteoporosis. METHODS: Relevant literature was retrieved in CNKI, WanFang, VIP, PubMed, and Web of Science databases using computers. The search terms were “osteoporosis, Piezo1, mechanical, osteoblast, osteoclast, chondrocyte, bone” in Chinese and English. Finally, 65 documents were included for review according to the inclusion and exclusion criteria. RESULTS AND CONCLUSION: The structure of Piezo1 has been continuously analyzed in the breakthrough of cryo-electron microscopy. Based on a three-bladed propeller 3D structure, Piezo1 exhibits different structural changes under silent and stressful states. Piezo1-mediated mechanical stress stimulation can affect bone formation by regulating the functions of osteoblasts, chondrocytes, endothelial cells and intestinal cells, and simultaneously affect bone resorption by regulating the function of osteoclasts, thereby playing an important role in anti-osteoporosis. Piezo1-mediated mechanical stress mainly affects bone formation by regulating the function of osteoblasts through the Wnt/β-catenin signaling pathway. And it has a two-way regulatory effect on osteoclasts due to different type, strength, and duration of mechanical force, which needs to be further quantified. For the use of Piezo1 in the treatment of osteoporosis, emphasis should be placed on clinical and animal model research for osteoporosis, osteoclast-related mechanisms, and new composite materials. Figures and Tables | References | Related Articles | Metrics

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Iron overload in bone diseases Li Miao, He Qi, Zeng Jiaxu, Chen Bohao, Li Shaocong, Pan Zhaofeng, Yang Junzheng, Xiao Jiacong, Wang Haibin 2023, 27 (17):  2723-2728.  doi: 10.12307/2023.145 Abstract ( 315 )   PDF (997KB) ( 97 )   Save BACKGROUND:  Iron is an essential metal for the human body. Its storage and transportation mechanism is complex, and various factors are involved in the balance of iron metabolism. When the metabolic balance is destroyed, iron overload in the body will produce a large number of reactive oxygen species and cytotoxicity and even lead to ferroptosis, resulting in functional dysfunction of tissues and organs. However, the current research on iron overload mainly focuses on cardiovascular, nervous system and tumor diseases, while the research on the imbalance of bone homeostasis caused by iron overload and its mechanism in bone diseases is still limited. OBJECTIVE: To review the recent studies on iron overload in bone diseases and provides new ideas for the treatment of bone diseases by reviewing the latest findings of iron overload in bone diseases. METHODS: The search terms “iron, iron overload, ferroptosis, osteoporosis, osteoarthritis, osteosarcoma, bone related diseases” in Chinese and English were used for the retrieval of literature published from January 1978 to January 2022 in CNKI, WanFang Database, PubMed, and Web of Science, respectively. A total of 1 085 articles were initially retrieved. According to the inclusion criteria, 79 articles were included for review. RESULTS AND CONCLUSION: Ferroptosis caused by iron overload has great potential in the treatment of bone diseases, but there are some limitations such as lack of clinical application data and lack of clinical trials. Research on ferroptosis caused by iron overload focuses on the enzyme binding to iron to produce reactive oxygen species and irons that directly participate in Fenton reaction to mediate reactive oxygen species accumulation. Ferroptosis, as an independent form of cell death, offers a new approach to treating these diseases, as well as the possibility of combining existing treatment options and helping to address drug resistance in some diseases. Iron overload is involved in the development of osteoporosis by inhibiting the activity and function of osteoblasts and promoting the differentiation and activation of osteoclasts. Iron overload accelerates the progression of osteoarthritis and promotes chondrocyte apoptosis and matrix degradation. Iron overload can induce ferroptosis, apoptosis and autophagy of osteosarcoma cells and inhibit their invasion ability. Studies on the mechanism of ferroptosis caused by iron overload provide a new target and direction for the treatment of bone diseases such as osteoporosis, osteoarthritis, and osteosarcoma. Figures and Tables | References | Related Articles | Metrics

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Exercise intervention improves hippocampal cognitive function by regulating insulin-like growth factor 1 Peng Zifu, Guo Xiangying, Fang Hongbo, He Yimin, Jiang Ning 2023, 27 (17):  2729-2738.  doi: 10.12307/2023.402 Abstract ( 441 )   PDF (918KB) ( 138 )   Save BACKGROUND: In neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, hippocampal cognitive impairment is often accompanied, which will seriously impact the quality of life of patients. A large number of studies have confirmed that exercise can benefit neural plasticity and cognitive function. In these processes, insulin-like growth factor-1 plays an important role. However, there is a lack of systematic and comprehensive understanding on the improvement of hippocampal cognitive function by exercise regulating insulin-like growth factor-1. OBJECTIVE: To summarize the process in which exercise improves hippocampal cognitive function by regulating insulin-like growth factor-1 and to explore the relevant mechanism. METHODS: The first author searched the Elsevier, Web of Science, PubMed, CNKI, VIP, and WanFang databases with “exercise, physical exercise, IGF-1, insulin-like growth factor-1, hippocampal cognitive function, cognitive neuroscience, apoptosis, synaptic plasticity, neurogenesis, cerebral inflammation” as English and Chinese keywords. The search time was up to May 2022. Relevant studies on exercise intervention and regulation of insulin-like growth factor-1 to improve hippocampal cognitive function were retrieved and 76 articles were finally included for review. RESULTS AND CONCLUSION: Exercise can improve hippocampal cognitive function by regulating the expression of insulin-like growth factor-1. The related mechanisms include: (1) Exercise inhibits apoptosis of hippocampal neurons, improves hippocampal synaptic plasticity, increases hippocampal neurogenesis,  inhibit the occurrence and development of brain inflammation, and  improves hippocampal cognitive function  by regulating insulin-like growth factor-1. (2) Both aerobic and resistance exercises have certainly regulatory effects on the expression of insulin-like growth factor 1. However, their regulatory effects are disturbed by various factors, such as exercise intensity, exercise time, and sex of subjects. (3) For aerobic exercise, short-term moderate-intensity exercise or acute high-intensity exercise can significantly change the expression of insulin-like growth factor-1. For resistance exercise, only short-term moderate-intensity resistance exercise or high-intensity resistance exercise can significantly influence the expression of insulin-like growth factor-1. (5) Considering that neurodegenerative diseases such as Alzheimer’s disease and mild cognitive impairment mostly occur in the elderly who are more difficult to carry out resistance exercise and prone to sports injury, aerobic exercise is preferred to improve their hippocampal cognitive function. (6) Most studies on the mechanism by which exercise regulates insulin-like growth factor-1 expression to improve hippocampal cognitive function are animal experiments and there are relatively few clinical studies and a lack of exact methods to formulate exercise programs. Therefore, the research on this aspect still needs to be further studied, which will provide more theoretical basis for exercise to improve the cognitive function of patients with neurodegenerative diseases.  Figures and Tables | References | Related Articles | Metrics

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Bone ring technique for restoration of dentition defects with bone deficiency Qi Yuhan, Shi Qianhui, An Zheqing, Liao Jian 2023, 27 (17):  2738-2744.  doi: 10.12307/2023.112 Abstract ( 329 )   PDF (908KB) ( 49 )   Save BACKGROUND: At present, bone defect after tooth loss due to periodontitis and trauma is common and the application of various kinds of bone augmentation techniques has partially solved these problems. However, various commonly used bone augmentation techniques have limitations to varying degrees. To alleviate the above-mentioned problems, an improved technique, bone ring technique, has been proposed to provide clinical workers with more options for bone augmentation. OBJECTIVE: To summarize and review the related research trends of bone ring technique and its clinical application.  METHODS: A computer-based search of PubMed, WanFang, VIP, and CBM was performed by the first author. The keywords were “dentition defect, bone augmentation, dental implants, bone defect, bone graft material, bone ring technique” in English and Chinese. The retrieval time was from January 1986 to February 2022. A total of 431 articles were initially retrieved followed by screening, analysis, and summarization, and 60 articles were finally included for literature review. RESULTS AND CONCLUSION: Bone ring technique with concurrent dental implantation can shorten treatment time and avoid secondary operation in patients. Moreover, due to the good mechanical properties, this method is more conducive to the reconstruction and recovery of soft and hard tissue morphology. However, there are also some limitations, such as poor fixation, insufficient bone mass to meet the needs of patients with severe bone defects, and unacceptability of opening a second surgical area. Therefore, more high-quality, long-term and large-sample follow-up studies are still needed to continuously improve the bone ring technique so that it can better cope with dental implantation treatment for various types of dentition defects and bone defects. Figures and Tables | References | Related Articles | Metrics

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Role of calcium ions in the pathogenesis of chronic fluorosis Tang Yujing, Lan Fengjun, Li Guangdi, Wang Jian, Liu Riguang 2023, 27 (17):  2745-2753.  doi: 10.12307/2023.408 Abstract ( 334 )   PDF (1403KB) ( 131 )   Save BACKGROUND: Disorders of calcium metabolism mediate the occurrence and development of chronic fluorosis, but the specific molecular mechanism has not been elucidated and there is little systematic discussion on the role of calcium ion (Ca2+) in the pathogenesis of chronic fluorosis. OBJECTIVE: To review the role of Ca2+ in chronic fluorosis, thereby providing new ideas and perspectives for the exploration of the molecular mechanism of chronic fluorosis and the development of targeted drugs. METHODS: “Ca2+, fluorosis, pathogenesis, calcium overload, oxidative stress, endoplasmic reticulum stress, mitochondrial damage, apoptosis” were used as Chinese and English keywords, and the relevant literatures included in PubMed database and CNKI database from January 2000 to January 2022 were retrieved. After removal of obsolete, repetitive and low-credibility documents, 110 documents were finally included.  RESULTS AND CONCLUSION: Ca2+ plays an important role in the pathogenesis of chronic fluorosis. The calcium paradox forms of low extracellular calcium caused by bone calcium metabolism disorder and of high intracellular calcium caused by intracellular Ca2+ metabolism disorder jointly induce the damage of fluoride to the bone and non-bone tissues. Intracellular Ca2+ metabolism disorder, with calcium overload as the core link, mediates the occurrence and development of chronic fluorosis. The specific process is as follows: fluorine promotes the production of chronic fluorosis through the inhibition of calcium transporters/enzymes in the plasma membrane and endoplasmic reticulum and the interference of gene expression levels. Cytoplasmic calcium is overloaded, thereby activating the downstream calcium signal transduction pathway, forming a unified negative regulatory network with multiple mechanisms, such as oxidative stress, endoplasmic reticulum stress, mitochondrial damage, and jointly inducing apoptosis in bone and soft tissue cells. In contrast, calcium agents and inhibitors that act on intracellular calcium-related targets (LTCC Cav1.2, NMDARs, and CaM-CAMKII) exert therapeutic effects by reversing fluoride-induced calcium paradoxes. Recovery from Ca2+ metabolism disorders is an important approach for treating chronic fluorosis. From another point of view, this not only provides an immediate theoretical basis for the current clinical application of calcium agents, but also provides new ideas and confidence for the development of drugs acting on calcium-related targets in the future. Figures and Tables | References | Related Articles | Metrics

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Bibliometrics and visual analysis of research in the field of rehabilitation for femoroacetabular impingement syndrome in the past decade Wang Suping, Qiu Demei, Fan Zhonghe, Hu Bo 2023, 27 (17):  2754-2762.  doi: 10.12307/2023.193 Abstract ( 293 )   PDF (1974KB) ( 154 )   Save BACKGROUND: Femoroacetabular impingement syndrome is one of the main causes of hip pain, and there is a lack of research in the field of rehabilitation for femoroacetabular impingement syndrome in China. OBJECTIVE: To present the research trends and research hotspots in the field of femoroacetabular impingement syndrome rehabilitation based on the Web of Science and Citespace software in the form of scientific data combined with atlas and to analyze research prospects and propose future research directions. METHODS: Keywords regarding femoroacetabular impingement syndrome rehabilitation from 2012 to 2021 were searched in the Web of Science Core Collection, and the results were bibliometrically analyzed. Citespace software was then used to conduct visually analyze countries, institutions, authors, journals, keywords and co-cited references. Finally, research trends and hotspots in the past 10 years were summarized. RESULTS AND CONCLUSION: Femoroacetabular impingement syndrome rehabilitation has gradually attracted the attention of scholars and the number of publications and citations has increased yearly, with the United States taking the lead. Chinese scholars have published fewer papers in this field and only have cooperative relations with Australian and American scholars. China’s influence in this field needs to be improved. Keyword and literature co-citation burst analyses indicate that the research trends are gait function in patients with femoroacetabular impingement syndrome, clinical efficacy of non-surgical treatment/conservative treatment/physiotherapy for femoroacetabular impingement syndrome, and the efficacy of hip arthroscopy vs. non-surgical treatment. The high-frequency co-citations, high centrality and cluster analyses indicate that the research hotspots in this field are exploring the diagnosis of pain due to femoroacetabular impingement syndrome, the short-, medium-, and long-term clinical effects of non-surgical treatment vs. hip arthroscopy, the rehabilitation effect of physiotherapy, the applicability of self-report scales, the rehabilitation scheme of femoroacetabular impingement syndrome with cartilage injury or glenoid lip injury and paying attention to their rehabilitation process, preventing femoroacetabular impingement syndrome from progressing to osteoarthritis. Based on the analysis of relevant literature in the past 10 years, this review details the future research directions in this field, including explorations on the clinical efficacy of non-surgical/surgical treatment, the middle- and long-term efficacy of non-surgical treatment vs. surgical treatment, the concurrent loss of femoroacetabular impingement syndrome, and randomized controlled trials on the prognosis and rehabilitation of femoroacetabular impingement syndrome.   Figures and Tables | References | Related Articles | Metrics

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Therapeutic mechanism of traditional Chinese medicine in the treatment of hormone-induced necrosis of the femoral head Wu Ruiqi, Cui Wei, Yang Qipei, Zhou Yi, Zhang Xuan 2023, 27 (17):  2763-2771.  doi: 10.12307/2023.403 Abstract ( 320 )   PDF (2281KB) ( 120 )   Save BACKGROUND: In recent years, there have been many studies on the prevention and treatment of femoral head necrosis with traditional Chinese medicine. A variety of single Chinese medicines, Chinese medicine monomers and Chinese medicine compounds can regulate bone metabolism, lipid metabolism, and oxidative stress by targeting signaling molecules. The prevention and treatment of femoral head necrosis by translation-related signaling pathways has become a research hotspot. OBJECTIVE: To expound the global research progress in hormone-induced femoral head necrosis treated with Chinese medicine, in order to provide some ideas for the treatment of hormone-induced femoral head necrosis. METHODS: CNKI, WanFang, VIP, SinoMed, PubMed, Embase, and Web of Science databases were searched with the search terms “glucocorticoids, avascular necrosis of the femoral head, ANFH, pathogenesis, signal path, Chinese medicine compound, oxidative stress” in Chinese and English. Literature was retrieved on Chinese medicine compounds and active ingredients for intervention of the signaling pathway related to hormone-induced femoral head necrosis. A total of 71 documents were included according to the inclusion and exclusion criteria. RESULTS AND CONCLUSION: Chinese medicine may treat hormone-induced femoral head necrosis through multiple signaling pathways. Total saponins of Panax notoginseng, total flavonoids of Rhizoma Drynariae, and resveratrol glucoside promote osteoblast proliferation and differentiation and inhibit osteoclast formation by regulating the level of β-catenin protein and the formation of β-catenin-TCF/LEF complex via the Wnt/β-catenin signaling pathway. Recipes for invigorating blood and reinforcing marrow, warming yang and tonifying kidney, and relieving bone bi-syndrome maintain osteoblast-osteoclast dynamic balance and bone homeostasis by regulating the OPG/RANK/RANKL pathway. Puerarin, salidroside, allicin, and icariin influence the proliferation and apoptosis of osseous cells and angiogenesis of microvascular endothelial cells in the femoral head via the PI3K/Akt signaling pathway. Ginsenosides can down-regulate the expressions of superoxide dismutase and catalase by interfering with the Keapl-Nrf2-ARE signaling pathway, thereby attenuating oxidative stress damage. Gastrodin, lutein, and astragaloside IV can promote the proliferation and differentiation of osteoblasts by intervening Nrf2/HO-1 signaling, thereby improving the level of oxidative substances. Naringin and polygonin balance the osteogenic/adipogenic differentiation of bone marrow mesenchymal stem cells via the Nrf2/ARE signaling pathway. Traditional Chinese medicine can regulate oxidative stress response of osteocytes, which is another important way to treat hormone-induced necrosis of the femoral head. Figures and Tables | References | Related Articles | Metrics

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Platelet-rich plasma meets the therapeutic needs of different articular cartilage defects Zhang Ziyu, Wang Yiming, Li Han, Wang Zhonghan, Lu Jialin, Xu Rui, Jin Hui 2023, 27 (17):  2772-2779.  doi: 10.12307/2023.067 Abstract ( 304 )   PDF (893KB) ( 119 )   Save BACKGROUND: Articular cartilage is a kind of hyaline cartilage that has poor self-repair ability. Traditional treatments can merely regenerate fibrocartilage in the defect area but not completely repair a cartilage defect. Hence, it is necessary to explore an effective therapy for cartilage defects through regenerating hyaline cartilage. Platelet-rich plasma is an autologous platelet-rich extract containing various growth factors that has been widely applied in the treatment of articular cartilage defects currently and has shown beneficial therapeutic effects on various types of articular cartilage defects. At present, platelet-rich plasma therapy is a promising treatment for articular cartilage defects. OBJECTIVE: To summarize the preparation, storage and activation of platelet-rich plasma, analyze the properties of platelet-rich plasma in treating different types of articular cartilage defects, and discuss the therapeutic effects of platelet-rich plasma in treating articular cartilage defects. METHODS: Related articles were searched in PubMed, Web of Science, and CNKI using the keywords of “platelet-rich plasma, articular cartilage, prepraration, mechanism, full-thickness cartilage defect, osteochondral defect, weight-bearing areas defect, hip, knee, ankle, osteoarthritis, rheumatoid arthritis in English and Chinese. The search time was from database inception to August 2021. Initially 225 articles were searched and 90 eligible articles were included in final analysis. RESULTS AND CONCLUSION: Platelet-rich plasma contains high concentrations of growth factors that can play roles in promoting chondrocyte proliferation, regulating cartilage matrix secretion, inducing stem cell proliferation and differentiation, forming a strong scaffold structure, reducing inflammation, lubricating rough articular surface and reducing immune response in vivo, which can meet the requirements for treating various types of cartilage defects. Platelet rich plasma has a good therapeutic effect on full-thickness cartilage defects, osteochondral defects, weight-bearing area cartilage defects, osteoarthritis, and rheumatoid arthritis. Platelet-rich plasma also has the potential to treat growth plate defects considering its curative effects on these abnormal conditions. Figures and Tables | References | Related Articles | Metrics

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Chinese expert consensus on neurorestorative therapy with cerebrospinal fluid administration (2022) 2023, 27 (17):  2780-2788.  doi: 10.12307/2023.442 Abstract ( 409 )   PDF (1087KB) ( 40 )   Save BACKGROUND: The nervous system is highly protected by the blood-brain barrier and the blood-cerebrospinal fluid barrier and the development and administration of neurorestorative drugs are still challenging. Therefore, the clinical therapeutic effects of most drugs are limited. Direct administration to the nervous system through the cerebrospinal fluid route is also an important clinical treatment strategy, but there is currently no unified clinical application standard. OBJECTIVE: To explain the current status of cerebrospinal fluid administration and the indications, specific methods and precautions in clinical practice, thereby popularizing the application and improving the clinical efficacy. METHODS: The Expert Committee of Neurorestoratology of Beijing Medical Doctor Association and the Professional Branch of Neurorestoratology of Guangdong Medical Doctor Association organized and compiled this expert consensus by organizing relevant expert seminars from various disciplines across the country. RESULTS AND CONCLUSION: Direct administration to the nervous system through the cerebrospinal fluid route for neurorestorative therapy has a wide range of clinical indications and application prospects. However, attention should be paid to the safety and efficiency of cerebrospinal fluid administration, the combination of compound formulations, the maximum tolerated dose and full informed consent during the application process. References | Related Articles | Metrics