
pmid: 27037019
Osteoarthritis (OA) is a degenerative joint disease affecting millions of people. The degradation and loss of type II collagen induced by proinflammatory cytokines secreted by chondrocytes, such as factor-α (TNF-α) is an important pathological mechanism to the progression of OA. Edaravone is a potent free radical scavenger, which has been clinically used to treat the neuronal damage following acute ischemic stroke. However, whether Edaravone has a protective effect in articular cartilage hasn't been reported before. In this study, we investigated the chondrocyte protective effects of Edaravone on TNF-α induced degradation of type Ⅱ collagen. And our results indicated that TNF-α treatment resulted in degradation of type Ⅱ collagen, which can be ameliorated by treatment with Edaravone in a dose dependent manner. Notably, it was found that the inhibitory effects of Edaravone on TNF-α-induced reduction of type Ⅱ collagen were mediated by MMP-3 and MMP-13. Mechanistically, we found that Edaravone alleviated TNF-α induced activation of STAT1 and expression of IRF-1. These findings suggest a potential protective effect of Edaravone in OA.
Dose-Response Relationship, Drug, Tumor Necrosis Factor-alpha, Free Radical Scavengers, Enzyme Activation, Chondrocytes, Edaravone, Matrix Metalloproteinase 13, Humans, Collagen Type II, Antipyrine, Cells, Cultured
Dose-Response Relationship, Drug, Tumor Necrosis Factor-alpha, Free Radical Scavengers, Enzyme Activation, Chondrocytes, Edaravone, Matrix Metalloproteinase 13, Humans, Collagen Type II, Antipyrine, Cells, Cultured
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