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

Abstract

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.

Keywords: Apoptosis; Gastrodin; Inflammation; NF-κB; Osteoarthritis.