Rheumatoid arthritis (RA) is a common chronic autoimmune disease, which seriously harms human health. The hyperplastic growth of fibroblast-like synoviocytes (FLSs) plays a key role in the pathogenesis of RA. However, the pathogenesis of RA remains unclear. In this experiment, we confirmed that Tumor necrosis factor alpha (TNF-α) could activate the autophagy of RA-FLSs. 3-Methyladenine (3-MA) and Chloroquine (CQ), two types of autophagy blocker, combined with TNF-α were used to treat FLSs. The results showed that this treatment caused a reduction in the level of autophagy-related protein, significant increases in the expression of apoptosis-related protein and the apoptosis rate, and significant inhibition of the proliferation-promoting ability of TNF-α. Ammonium pyrrolidinedithiocarbamate (PDTC), a specific nuclear factor kappa-B (NF-κB) activity blocker, significantly inhibited autophagy induced by TNF-α. Collectively, these findings showed, for the first time, that TNF-α can up-regulate autophagy activity and activate the NF-κB signal pathway. Inhibition of autophagy can improve the imbalance of proliferation/apoptosis of FLSs aggravated by TNF-α to some extent, thus delaying the progression of RA. The NF-κB signal pathway may be involved in the regulation of FLSs autophagy by TNF-α.

类风湿关节炎（RA）是一种常见的慢性自身免疫性疾病，严重危害人类健康。成纤维细胞样滑膜细胞 (FLS) 的增生性生长在 RA 的发病机制中起关键作用。然而，RA的发病机制仍不清楚。在本实验中，我们证实了肿瘤坏死因子 α (TNF-α) 可以激活 RA-FLSs 的自噬。3-甲基腺嘌呤 (3-MA) 和氯喹 (CQ) 这两种自噬阻滞剂与 TNF-α 联合用于治疗 FLS。结果表明，该处理引起自噬相关蛋白水平降低，凋亡相关蛋白表达和凋亡率显着增加，显着抑制TNF-α的促增殖能力。吡咯烷二硫代氨基甲酸铵（PDTC），一种特定的核因子 kappa-B (NF-κB) 活性阻断剂，显着抑制 TNF-α 诱导的自噬。总的来说，这些发现首次表明 TNF-α 可以上调自噬活性并激活 NF-κB 信号通路。抑制自噬可在一定程度上改善TNF-α加重的FLSs增殖/凋亡失衡，从而延缓RA的进展。NF-κB信号通路可能参与了TNF-α对FLSs自噬的调节。