骨髓间充质干细胞与成纤维细胞样滑膜细胞(RA-FLS)共培养通过抑制炎症反应减轻类风湿关节炎细胞凋亡

IF 0.1 4区 医学
qingchen liang, Yanjie Tian, Zijin Liu, Dejun Yu, Hengbing Guo, Fenglong Sun
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引用次数: 0

摘要

目的:研究骨髓间充质干细胞(bmsc)对RA成纤维细胞样滑膜细胞(FLS)和胶原诱导性关节炎(CIA)的影响,并进一步探讨其作用机制。方法:建立类风湿性关节炎细胞模型,并与BMSC共培养。MTT法和流式细胞仪检测细胞增殖和凋亡,ELISA法检测细胞中炎症因子的表达水平,western印迹法分析相关途径中蛋白质的磷酸化激活和表达。结果:bmsc抑制了TNF-a诱导的RA-FLS的增殖,增加了细胞凋亡率,并上调了胱天蛋白酶-3、PARP和Burlington水平。同时抑制il-10、il-1β和il-6的表达。p-STAT3水平以剂量依赖性方式下调。STAT3的过表达部分中和BMSC介导的胱天蛋白酶-3增加和PARP剪切,以及il-10、il-1B和il-6的下调。这表明骨髓基质干细胞使STAT3通路失活。此外,骨髓基质干细胞可以有效抑制RA-FLS和CIA大鼠模型中炎性细胞因子的产生。结论:总之,合成是一种潜在的类风湿性关节炎长期治疗药物,它可以通过灭活STAT3途径在类风湿性关节病中发挥治疗作用。同时,揭示了STAT3通路在类风湿性关节炎发病机制中的作用,并提示STAT3通路作为类风湿性关节病治疗靶点的可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Co-Culture of Bone Marrow Mesenchymal Stem Cells and Fibroblast-Like Synoviocytes (RA-FLS) Alleviates Rheumatoid Arthritis Cell Apoptosis by Inhibiting Inflammatory Response
Objective: To investigate the effect of bone marrow mesenchymal stem cells (bmsc) on RA-fibroblast-like synovial cells (FLS) and collagen-induced arthritis (CIA), and to further explore the mechanism of action. Methods: The rheumatoid arthritis cell model was established, and the cells were co-cultured with BMSC. The proliferation and apoptosis of the cells were detected by MTT and flow cytometry, the expression level of inflammatory factors in the cells was detected by ELISA, and the phosphorylation activation and expression of proteins in related pathways were analyzed by western blotting. Results: bmsc inhibited the proliferation of TNF-a-induced RA-FLS, increased the apoptosis rate, and up-regulated caspase-3, PARP and Burlington levels. Meanwhile, the expression of il-10, il-1β and il-6 was inhibited. p-STAT3 levels were down-regulated in a dose-dependent manner. Overexpression of STAT3 partially neutralizes BMSC-mediated caspase-3 increase and PARP shear, as well as down-regulation of il-10, IL-1B, and il-6. This suggests that BMSCs inactivate the STAT3 pathway. In addition, BMSCs can effectively inhibit the production of inflammatory cytokines in rat models of RA-FLS and CIA. Conclusions: In summary, synthesis is a potential long-term treatment drug for rheumatoid arthritis, which can play a therapeutic role in rheumatoid arthritis by inactivating the STAT3 pathway. At the same time, it reveals the role of STAT3 pathway in the pathogenesis of rheumatoid arthritis, and suggests the possibility of STAT3 pathway as a therapeutic target for rheumatoid arthritis.
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