Abstract Title:

Gastrodin reduces IL-1β-induced apoptosis, inflammation, and matrix catabolism in osteoarthritis chondrocytes and attenuates rat cartilage degeneration in vivo.

Abstract Source:

Biomed Pharmacother. 2018 Jan ;97:642-651. Epub 2017 Nov 6. PMID: 29101808

Abstract Author(s):

Jian Chen, Yun-Tao Gu, Jun-Jun Xie, Cong-Cong Wu, Jun Xuan, Wei-Jun Guo, Ying-Zhao Yan, Long Chen, Yao-Sen Wu, Xiao-Lei Zhang, Jian Xiao, Xiang-Yang Wang

Article Affiliation:

Jian Chen


Therapeutics for osteoarthritis (OA) are intended to restore chondrocyte function and inhibit cell apoptosis. Previous studies have shown that gastrodin had anti-apoptotic and anti- inflammatory effects. However, little is known about whether gastrodin has protective effects against the processes of OA. We studied the potential effects of gastrodin on chondrocytes and the underlying mechanisms. Our results showed that gastrodin could prevent chondrocyte apoptosis induced by IL-1β. Additionally, gastrodin suppressed the nuclear factor kappa B (NF-κB) pathway, decreased the release of inflammatory mediators (IL-6, TNF-α), and reduced matrix catabolism in IL-1β-treated chondrocytes. Furthermore, gastrodin ameliorated rat cartilage degeneration in an OA model of knee joints in vivo, suggesting its potential as a candidate therapeutic for OA.

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