Introduction. Chondrocyte apoptosis is considered one of the pathogenic factors of osteoarthritis (OA), but its importance in the pathogenesis of OA remains unclear. Recent research adds progress to the knowledge that the mitochondrial signaling pathway mediates chondrocyte apoptosis in OA. Method. Rat chondrocyte exposed to H₂O₂ was used as the experimental oxidative stress model. Chondrocyte viability was tested by cell counting kit-8 (CCK-8) assay. Cell apoptosis and ROS were tested by flow cytometry. Contents of malondialdehyde (MDA), catalase (CAT), caspase-3, caspase-9, cytochrome C, superoxide dismutase (SOD)-2, and adenosine triphosphate (ATP) were evaluated by biochemical detection. The expressions of related genes and proteins were assessed by quantitative polymerase chain reaction (qPCR) and western blot. Results. H₂O₂ provokes oxidative stress and decreases the viability of chondrocyte, which leads to the release of cytochrome C and inhibition of SOD-2 activity. The damage of mitochondrion disturbs the energy metabolism of chondrocyte and eventually induces chondrocyte apoptosis through the mitochondrial pathway. Furthermore, pretreated with anglicasinensis polysaccharide (ASP) or caspase inhibitors increase the expression of Bcl-2 and Bcl-xL but do not work for the expression of Bax and Bad. Conclusion. Oxidative stress induces chondrocyte apoptosis through caspase-dependent and caspase-independent mitochondrial pathways. ASP protects chondrocyte from H₂O₂-induced oxidative stress and subsequent cell injury through its antioxidant effect by inhibiting the caspase pathway.

中文翻译：

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氧化应激通过依赖半胱天冬酶和非半胱天冬酶依赖的线粒体途径和当归多糖的抗氧化机制诱导软骨细胞凋亡

简介。软骨细胞凋亡被认为是骨关节炎（OA）的致病因素之一，但其在OA发病机制中的重要性仍不清楚。最近的研究增加了线粒体信号通路介导 OA 中软骨细胞凋亡的认识。方法。暴露于 H ₂ O _{2的大鼠软骨细胞}用作实验氧化应激模型。通过细胞计数试剂盒 8 (CCK-8) 测定法测试软骨细胞活力。流式细胞仪检测细胞凋亡和活性氧。通过生化检测评估丙二醛（MDA）、过氧化氢酶（CAT）、caspase-3、caspase-9、细胞色素C、超氧化物歧化酶（SOD）-2和三磷酸腺苷（ATP）的含量。通过定量聚合酶链反应（qPCR）和蛋白质印迹评估相关基因和蛋白质的表达。结果。H ₂ O ₂引起氧化应激并降低软骨细胞的活力，导致细胞色素 C 的释放和 SOD-2 活性的抑制。线粒体的损​​伤扰乱了软骨细胞的能量代谢，最终通过线粒体途径诱导软骨细胞凋亡。此外，用 anglicasinensis 多糖 (ASP) 或半胱天冬酶抑制剂预处理可增加 Bcl-2 和 Bcl-xL 的表达，但对 Bax 和 Bad 的表达不起作用。结论。氧化应激通过半胱天冬酶依赖性和半胱天冬酶非依赖性线粒体途径诱导软骨细胞凋亡。ASP 保护软骨细胞免受 H ₂ O _2的伤害-通过抑制半胱天冬酶途径的抗氧化作用诱导氧化应激和随后的细胞损伤。