Kaempferol inhibits interleukin‑1β stimulated matrix metalloproteinases by suppressing the MAPK‑associated ERK and P38 signaling pathways

山奈酚通过抑制 MAPK 相关的 ERK 和 P38 信号通路来抑制白细胞介素 1β 刺激的基质金属蛋白酶

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作者:Xiaojian Huang, Qiyong Pan, Zekai Mao, Pengcheng Wang, Rui Zhang, Xiaohu Ma, Jingyuan Chen, Hongbo You

Abstract

Osteoarthritis (OA) is a common degenerative joint disease in older adults. A number of previous studies have demonstrated that natural flavonoids can serve as promising therapeutic drugs for OA. Kaempferol, a phytochemical ingredient mainly present in various fruits, has exhibited its prominent anti‑inflammatory and antioxidant effects in numerous diseases. However, whether Kaempferol ameliorates the deterioration of arthritis remains to be elucidated. The aim of the present study was to investigate the therapeutic role of Kaempferol on OA in rat chondrocytes. The results revealed that Kaempferol significantly inhibited the interleukin (IL)‑1β‑induced protein expression of inflammatory mediators such as inducible nitric oxide synthase and cyclo‑oxygenase‑2. In addition, the common matrix degrading enzymes [matrix metalloproteinase (MMP)‑1, MMP‑3, MMP‑13 and a disintegrin and metalloproteinase with thrombospondin motif‑5] induced by IL‑1β were also suppressed by Kaempferol, and consequently abolished the degradation of collagen II. Furthermore, the anti‑inflammatory effect of Kaempferol was mediated by the inhibition of the mitogen activated protein kinase‑associated extracellular signal‑regulated kinase and P38 signaling pathways. These results collectively indicated that Kaempferol can potentially prevent OA development and serve as a novel pharmacological target in the treatment of OA.

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