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find Author "TIANFaming" 5 results
  • RESEARCH PROGRESS OF EFFECTS OF STRONTIUM RANELATE ON OSTEOARTHRITIS

    ObjectiveTo review the research progress focused on the effects of strontium ranelate (SR) on osteoarthritis. MethodsThe relevant literature about the effects and mechanism of SR intervening osteoarthritis in recent years was extensively reviewed and comprehensively analyzed. ResultsSR not only could improve the microenvironment of bone metabolism in articular cartilage with osteoarthritis, promote activity of osteoblasts, and inhibit activity of osteoclasts, but also could adjust the expression of key proteases which affect cartilage formation, and therefore it has a potential protective effect on subchondral bone during the progression of osteoarthritis cartilage. ConclusionSR is expected to become a drug of osteoarthritis disease remission, but further studies are needed to clarify the mechanism of SR in osteoarthritis, and finally confirm the best application dosage of SR in osteoarthritis treatment.

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  • PROGRESS IN DISC DEGENERATION MODELS AND CALCITONIN THERAPY

    ObjectiveTo review the disc degeneration models and the current treatment status of calcitonin. MethodsRecent literature concerning the disc degeneration models and the calcitonin treatment of disc degeneration was extensively reviewed and summarized. ResultsDifferent models of disc degeneration have advantages and disadvantages; calcitonin can relieve disc degeneration at different degrees in vitro and in vivo studies. ConclusionDisc degeneration model for the study of disc degeneration mechanism offers a variety of ideas,and the results of calcitonin treatment in the disc degeneration model can provide the basis for future experiments.

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  • REGUL ATORY EFFECT OF SIMVASTATIN ON MIDDLE/L ATE STAGES OSTEOGENIC DIFFERENTIATION OF BONE MARROW MESENCHYMAL STEM CELLS VIA p38MAPK PATHWAY

    ObjectiveTo investigate the regulatory effect of simvastatin on osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) at middle/late stages by p38MAPK pathway under condition of osteoinductive environment. MethodsThe bone marrow of bilateral femur and tibia were harvested from 20 4-week-old female Sprague Dawley rats. BMSCs were isolated and cultured with whole bone marrow culture method; the second generation of cells were randomly divided into 5 groups: control group (complete medium, CM), simvastatin group (simvastatin medium, SIM), osteogenic induction group (osteogenic induction medium, OM), simvastatin and osteogenic induction group (simvastatin+osteogenic induction medium, OM+SIM), and blocker group (SB203580+simvastatin+osteogenic induction medium, OM+SIM+SB). MTT assay was used to detect the cell activity in CM group and SIM group at 2, 3, 4, 5, and 6 days, ELISA method to measure the content of alkaline phosphatase (ALP) in OM group and OM+SIM group at 7 and 14 days. The mRNA and protein expressions of osteocalcin (OCN) were detected by real-time quatitative PCR and Western blot after 1, 12, and 24 hours of osteogenic induction at 21 and 28 days. The protein expressions of phospho-p38 (p-p38) and p38 in OM group, OM+SIM group, and OM+SIM+SB group were detected by Western blot at the best induction time of simvastatin. ResultsMTT assay showed that no significant difference was found in absorbance (A) value between CM group and SIM group at each time point (P > 0.05), indicating no effect of 1×10-7 mol/L simvastatin on cell viability. ELISA results showed that ALP content significantly increased in OM+SIM group when compared with OM group at 7 and 14 days; the ALP content was significantly higher at 7 days than 14 days in OM group and OM+SIM group (P < 0.05). OCN mRNA and protein expressions at 12 hours were significantly higher than those at other time points in each group (P < 0.05), and the expressions of OM+SIM group was significantly higher than those of OM group (P < 0.05). The best induction time of simvastatin was 12 hours. At 12 hours after blocking intervention, the p-p38/p38 in OM+SIM+SB group was significantly lower than that in OM group and OM+SIM group (P < 0.05), and the p-p38/p38 in OM+SIM group was significantly higher than that in OM group (P < 0.05). ConclusionSimvastatin can increase the mRNA and protein expression levels of OCN and the protein of p-p38 in osteogenic differentiation of BMSCs at middle/ late stages, and its best induction time is 12 hours.

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  • RESEARCH PROGRESS OF Hedgehog SIGNALING PATHWAY IN REGULATING BONE FORMATION AND OSTEOGENIC DIFFERENTIATION OF BONE MESENCHYMAL STEM CELLS

    ObjectiveTo summarize the research progress of the effects and mechanisms of Hedgehog signaling pathway in regulating bone formation and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). MethodsThe related literature concerning the regulations and mechanism of Hedgehog signaling pathway in osteogenic differentiation of BMSCs and bone formation in vivo, in vitro, and ex vivo studies in recent years was analyzed and summarized. ResultsThe in vitro studies indicate that Hedgehog signaling pathway can promote osteogenic differentiation of BMSCs via activation of key molecules Smoothened (Smo) and Gli1 which are downstream of Hedgehog signaling, and Hedgehog signaling can activate mTORC2-Akt signaling by upregulation of insulin-like growth factor which has similar effects. Hedgehog signaling regulates osteoblast differentiation via activation of Hh-Smo-Ptch1-Gli signaling pathway and inhibition of Hh-Gαi-RhoA stress fibre signaling. Hedgehog signaling can regulate key molecules of osteogenesis Runx2 for promoting osteogenic differentiation and matrix mineralization by synergism of bone morphogenetic protein and Wnt signaling, and promotes bone formation and repair and healing for bone defect and bone graft model in vivo. ConclusionHedgehog signaling can regulate bone formation and osteogenic differentiation of BMSCs via activation of Hedgehog signaling and other signaling pathways. Hedgehog signaling pathway may be a potential target for developing treatment for bone related diseases of osteoporosis and fracture healing disorders.

    Release date:2016-12-12 09:20 Export PDF Favorites Scan
  • VERTEBRAL SUBCHONDRAL BONE AND INTERVERTEBRAL DISC DEGENERATION

    ObjectiveTo review the role of vertebral subchondral bone in maintaining normal physiological function of the intervertebral disc and in the intervertebral disc degeneration in light of bone anatomy, microstructure, histopathological features, and MRI imaging features. MethodsThe related home and abroad literature concerning vertebral subchondral bone and intervertebral disc degeneration was extensively reviewed and comprehensively analyzed. ResultsVertebral subchondral bone is part of the vertebral endplate and is defined as the vascularized cortical and trabecular bone layer located between the cartilage endplate and vertebral body. It not only plays a cushion shocks role in terms of conducting stress and effectively resists the hydrostatic nucleus, but also ensures the normal supply of disc nutrition. Subchondral bone sclerosis caused by bone remodeling abnormality severely decreases the ability of subchondral bone stress absorption and protective function of disc, which finally leads to increased inflammatory factors locally and hindered nutrition pathway of disc and enhanced disc degeneration. ConclusionTo further strengthen the knowledge and understanding of the vertebral subchondral bone will play a positive role in the study on the pathogenesis of intervertebral disc degeneration.

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