PI3K/AKT/mTOR通路
炎症
蛋白激酶B
肿瘤坏死因子α
细胞凋亡
类风湿性关节炎
成纤维细胞
基质金属蛋白酶
癌症研究
关节炎
化学
白细胞介素6
信号转导
细胞生长
促炎细胞因子
白细胞介素
细胞因子
药理学
医学
免疫学
生物化学
体外
摘要
Rheumatoid arthritis (RA) is a complex chronic inflammatory disease that is associated with the aberrant activation of fibroblast‐like synoviocytes (FLS). Kaempferitrin is a natural flavonoid glycoside that possesses anti‐inflammatory bioactivity. However, the effect of kaempferitrin on RA has not yet been revealed. The aim of the present study was to investigate the effect of kaempferitrin on human RA‐FLS MH7A cell line. We found that kaempferitrin inhibited proliferation and induced apoptosis of MH7A cells. Kaempferitrin decreased the levels of interleukin (IL)‐1β, IL‐6, tumor necrosis factor (TNF)‐α, matrix metalloproteinase (MMP)‐1, and MMP‐3 in MH7A cells. Moreover, kaempferitrin blocked the activation of nuclear factor‐κB (NF‐κB) and protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathways. Furthermore, treatment with kaempferitrin decreased paw thickness and arthritis scores, and reduced the serum levels of IL‐1β, IL‐6, and TNF‐α in a collagen‐induced arthritis mouse model. In conclusion, kaempferitrin inhibited cell proliferation, induced cell apoptosis, and ameliorated inflammation of RA‐FLS by suppressing the NF‐κB and Akt/mTOR pathways.
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