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Effects of autophagy on apoptosis of articular chondrocytes in adjuvant arthritis rats

机译:自噬对佐剂关节炎大鼠关节软骨细胞凋亡的影响。

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摘要

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease that eventually leads to joint deformities and loss of joint function. Previous studies have demonstrated a close relationship between autophagy and the development of RA. Although autophagy and apoptosis are two different forms of programmed death, the relationship between them in relation to RA remains unclear. In this study, we explored the effect of autophagy on apoptosis of articular chondrocytes in vivo and in vitro. Adjuvant arthritis (AA) and acid‐induced primary articular chondrocyte apoptosis were used as in vivo and in vitro models, respectively. Articular chondrocyte autophagy and apoptosis were both observed dynamically in AA rat articular cartilage at different stages (15 days, 25 days and 35 days). Moreover, chondrocyte apoptosis and articular cartilage injury in AA rats were increased by the autophagy inhibitor 3‐methyladenine (3‐MA) and decreased by the autophagy activator rapamycin. In addition, pre‐treatment with 3‐MA increased acid‐induced chondrocyte apoptosis, while pre‐treatment with rapamycin reduced acid‐induced chondrocyte apoptosis in vitro. These results suggest that autophagy might be a potential target for the treatment of RA.
机译:类风湿关节炎(RA)是一种慢性全身性自身免疫性疾病,最终导致关节畸形和关节功能丧失。先前的研究表明自噬与RA的发展之间存在密切的关系。尽管自噬和细胞凋亡是程序性死亡的两种不同形式,但它们与RA的关系仍不清楚。在这项研究中,我们探讨了自噬在体内和体外对关节软骨细胞凋亡的影响。佐剂性关节炎(AA)和酸诱导的原发性软骨细胞凋亡分别用作体内和体外模型。在不同阶段(15天,25天和35天)在AA大鼠关节软骨中动态观察到关节软骨细胞自噬和凋亡。此外,自噬抑制剂3-甲基腺嘌呤(3-MA)会增加AA大鼠的软骨细胞凋亡和关节软骨损伤,而自噬激活剂雷帕霉素会降低软骨细胞凋亡和关节软骨损伤。此外,用3-MA预处理可增加酸诱导的软骨细胞凋亡,而用雷帕霉素预处理可减少酸诱导的体外软骨细胞凋亡。这些结果表明自噬可能是治疗RA的潜在目标。

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