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目的:探讨脂联素对类风湿关节炎(RA)滑膜成纤维细胞合成分泌MMP-3的影响机制。方法:购买培养类风湿关节炎滑膜成纤维细胞(MH7A),给予脂联素刺激,观察不同浓度及时间下MMP-3mRNA及蛋白的合成分泌情况;随后通过NF-κB抑制剂检测最常见的炎性通路NF-κB是否参与了本调控;最后采用慢病毒基因沉默的手段,检测NF-κB通路的亚基p65和IKKβ的参与情况。结果:脂联素促进人滑膜成纤维细胞中MMP-3mRNA和蛋白的表达,并呈时间、剂量依赖效应。脂联素是通过NF-κB通路参与调控人滑膜成纤维细胞中MMP-3的表达,NF-κB通路中p65和IKKβ介入了脂联素对MMP-3的调控。结论:脂联素通过NF-κB(p65,IKKβ)通路促进类风湿关节炎滑膜成纤维细胞MMP-3的表达,提示脂联素可能为RA的前炎性因子,参与了RA的发生发展。
Objective: To investigate the mechanism of adiponectin on the synthesis and secretion of MMP-3 in rheumatoid arthritis (RA) synovial fibroblasts. Methods: The cultured rheumatoid arthritis synovial fibroblasts (MH7A) were purchased and stimulated with adiponectin to observe the synthesis and secretion of MMP-3 mRNA and protein at different concentrations and time. The most common NF-κB inhibitor NF-κB is involved in the regulation of the inflammatory pathway; Finally, the use of lentiviral gene silencing means NF-κB pathway subunits p65 and IKKβ participation. Results: Adiponectin promoted the expression of MMP-3 mRNA and protein in human synovial fibroblasts in a time-and dose-dependent manner. Adiponectin is involved in the regulation of MMP-3 expression in human synovial fibroblasts through the NF-κB pathway, and p65 and IKKβ in the NF-κB pathway are involved in the regulation of MMP-3 by adiponectin. CONCLUSION: Adiponectin promotes the expression of MMP-3 in rheumatoid arthritis synovial fibroblasts through NF-κB (p65, IKKβ) pathway, suggesting that adiponectin may be a proinflammatory factor of RA and is involved in the development of RA .