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首页> 外文期刊>Cellular Physiology and Biochemistry >Mitomycin C Induces Apoptosis in Rheumatoid Arthritis Fibroblast-Like Synoviocytes via a Mitochondrial-Mediated Pathway
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Mitomycin C Induces Apoptosis in Rheumatoid Arthritis Fibroblast-Like Synoviocytes via a Mitochondrial-Mediated Pathway

机译：丝裂霉素C通过线粒体介导的途径诱导类风湿关节炎成纤维样滑膜细胞凋亡

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Background/Aims: Rheumatoid arthritis (RA) is a systemic chronic inflammatory disease characterised by prominent synoviocyte hyperplasia and a potential imbalance between the growth and death of fibroblast-like synoviocytes (FLS). Mitomycin C (MMC) has previously been demonstrated to inhibit fibroblast proliferation and to induce fibroblast apoptosis. However, the effects of MMC on the proliferation and apoptosis of human RA FLS and the potential mechanisms underlying its effects remain unknown. Methods: Cell viability was determined using the Cell Counting Kit-8 assay. Apoptotic cell death was analysed via Annexin V-FITC/PI double staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling. The production of intracellular reactive oxygen species (ROS) was assessed via flow cytometry, and the changes in mitochondrial membrane potential (ΔΨm) were visualized based on JC-1 staining via fluorescence microscopy. The expression of apoptosis-related proteins was determined via Western blot. Results: Treatment with MMC significantly reduced cell viability and induced apoptosis in RA FLS. Furthermore, MMC exposure was found to stimulate the production of ROS and to disrupt the ΔΨm compared to the control treatment. Moreover, MMC increased the release of mitochondrial cytochrome c, the ratio of Bax/Bcl-2, the activation of caspase-9 and caspase-3, and the subsequent cleavage of poly(ADP-ribose) polymerase. Conclusion: Our findings suggest that MMC inhibits cell proliferation and induces apoptosis in RA FLS, and the mechanism underlying this MMC-induced apoptosis may involve a mitochondrial signalling pathway.
机译：背景/目的：类风湿关节炎（RA）是一种系统性慢性炎性疾病，其特征是滑膜细胞增生明显，成纤维样滑膜细胞（FLS）的生长与死亡之间可能存在不平衡。丝裂霉素C（MMC）先前已证明抑制成纤维细胞增殖并诱导成纤维细胞凋亡。然而，MMC对人RA FLS增殖和凋亡的影响及其潜在的潜在机制仍然未知。方法：使用细胞计数试剂盒8测定法测定细胞活力。通过膜联蛋白V-FITC / PI双重染色和末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记分析凋亡细胞的死亡。通过流式细胞术评估细胞内活性氧（ROS）的产生，基于JC-1染色，通过荧光显微镜观察线粒体膜电位（ΔΨm）的变化。通过Western印迹确定凋亡相关蛋白的表达。结果：MMC处理可显着降低RA FLS的细胞活力并诱导其凋亡。此外，与对照处理相比，发现MMC暴露可刺激ROS的产生并破坏ΔΨm。此外，MMC增加了线粒体细胞色素c的释放，Bax / Bcl-2的比率，caspase-9和caspase-3的活化以及随后的多聚ADP-核糖聚合酶的裂解。结论：我们的发现表明MMC抑制RA FLS的细胞增殖并诱导细胞凋亡，而这种MMC诱导的细胞凋亡的潜在机制可能涉及线粒体信号传导途径。

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