Mangiferin Prevents TBHP-Induced Apoptosis and ECM Degradation in Mouse Osteoarthritic Chondrocytes via Restoring Autophagy and Ameliorates Murine Osteoarthritis

Abstract EN

Osteoarthritis (OA) is an age-related degenerative disease with complicated pathology involving chondrocyte apoptosis and extracellular matrix (ECM) degradation.

Previous studies have shown that moderate autophagy has a protective effect against apoptosis in chondrocyte.

Mangiferin is a natural polyphenol and exerts multiple pharmacological effects on different diseases in various preclinical studies.

In this study, we investigated the effects of mangiferin on OA and delineated a potential molecular mechanism.

In vitro, mangiferin treatment inhibited the expression of proapoptotic proteins induced by tert-butyl hydroperoxide (TBHP), increased the expression of antiapoptotic Bcl-2, and prevented ECM degradation by inhibiting the production of matrix-degrading enzyme.

Mechanistically, mangiferin enhanced autophagy by activating the AMP-activated protein kinase (AMPK) signaling pathway.

On the contrary, inhibition of autophagy partly abolished the protective effects of mangiferin on antiapoptosis and ECM synthesis in TBHP-treated chondrocyte.

Correspondingly, the protective effect of mangiferin was also found in a mouse OA model.

In conclusion, our results suggested that mangiferin serves as a potentially applicable candidate for treating OA.