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作 者:谷远洋[1] 严培军[1] GU Yuanyang;YAN Peijun(Affiliated Hospital of Nanjing University of Chinese Medicine,Nanjing,210029,China)
机构地区:[1]南京中医药大学附属医院,江苏南京210029
出 处:《南京中医药大学学报》2018年第4期357-360,共4页Journal of Nanjing University of Traditional Chinese Medicine
基 金:江苏省中医药局科技项目(ZD201706)
摘 要:目的研究人参皂苷Rg1对IL-1β诱导的人膝软骨降解的保护作用及其分子机制。方法收集OA病人滑膜及软骨组织,培养成纤维滑膜细胞(FLS),采用IL-1β激发FLS细胞并与软骨骨片共培养,设空白对照组,IL-1β组(20ng/mL)为阳性对照组,不同浓度Rg1(0、5、50μmol/L)+IL-1β(20ng/mL)为实验组。用番红O染色观察软骨降解情况,qPCR分析MMPs相关基因表达情况,ELISA法检测上清液中MMP-3表达情况,Western blot分析Rg1对OA-FLS细胞中NF-κB通路中相关蛋白的调控。结果 Rg1可以显著抑制IL-1β诱导的软骨降解,发挥软骨保护作用。Rg1对软骨保护作用主要通过抑制成纤维滑膜细胞中MMPs表达,其中主要抑制MMP-3基因和蛋白表达,且该作用可能与Rg1调控NF-κB通路有关。结论人参皂苷Rg1可以抑制IL-1β诱导的软骨降解,发挥软骨保护作用,主要通过抑制FLS中MMP-3基因和蛋白表达。OBJECTIVE To investigate the inhibition effects and underlying mechanism of Ginsenoside Rg1 on IL-1β induced cartilage degradation. METHODS The synovial membrane and cartilage tissue of Osteoarthritis patients were collected and cultured into fibroblast synoviocytes. The FLS cells were stimulated by IL-1β and co cultured with chondrocytes. We divided the experiment into different groups, including the blank group, the IL-1β group and the different concentration Rg1 groups. We observed the degradation of cartilage tissue was observed by staining with red O, and real time fluorescence quantitative PCR was used to analyze the gene expression of MMPs, and the expression of MMP 3 in the supernatant was detected by ELISA, also the Western blot analysis was employed to determine the related proteins in NF κB pathway. RESULTS Rg1 significantly inhibited the degradation of cartilage induced by IL-1β to protect the cartilage. The protective effect of Rg1 on cartilage was mainly contributed to its inhibition on MMPs, especially by inhibiting the MMP 3 gene and protein expression in the synovial fibroblasts. Rg1 inhibited the expression of MMP 3 mainly through NF κB pathway. CONCLUSION Rg1 can inhibit the cartilage degradation induced by IL-1β and play the role of cartilage protection, mainly by inhibiting the expression of MMP 3 gene and protein in FLS.
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