A synergistic effect of triptolide and curcumin on rheumatoid arthritis by improving cell proliferation and inducing cell apoptosis via inhibition of the IL-17/NF-κB signaling pathway

雷公藤甲素 姜黄素 细胞凋亡 类风湿性关节炎 细胞生长 信号转导 NF-κB 肿瘤坏死因子α 药理学 癌症研究 关节炎 化学 炎症 医学 免疫学 生物化学
作者
Chaofeng Zhang,Yiyang Weng,Haibin Wang,Siting Zhan,Chaoqi Li,Donghui Zheng,Lin Qi
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:142: 112953-112953 被引量:12
标识
DOI:10.1016/j.intimp.2024.112953
摘要

Rheumatoid arthritis (RA) is a chronic, progressive, systemic autoimmune disease. While triptolide (TPL) and curcumin (CUR) are known to have multiple beneficial effects on RA, the combined effect of TPL and CUR remains unexplored. This study aimed to investigate their synergistic effect on cell proliferation and apoptosis via the IL-17/NF-κB signaling pathway. The collagen-induced arthritis (CIA) rat model was established, showing severe joint and synovial damage compared to normal rats. Treatment with TPL and CUR reduced the severity of RA in the CIA rat model and alleviated serum inflammatory cytokines, such as rheumatoid factor, IL-17, TNF-α, IL-1β, and IL-6. The elevated levels of IL-17 and NF-κB in CIA rats were also inhibited, and the resistant apoptosis was aggravated by TPL and CUR. In vitro, the improvement of cell proliferation and induction of apoptosis were observed in LPS-stimulated MH7A cells treated with TPL and CUR, associated with the inhibition of the IL-17/NF-κB signaling pathway. Taken together, a synergistic effect of TPL and CUR on RA may involve relieving symptoms, improving excessive proliferation, inducing apoptosis resistance, and inhibiting the IL-17/NF-κB signaling pathway.
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