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

  • Oxid Med Cell Longev. 2019 Oct 15;2019:8783197. doi: 10.1155/2019/8783197.
Yao Li  1  2  3 ,  Yaosen Wu  1 ,  Kaixia Jiang  3 ,  Wen Han  2 ,  Jing Zhang  2 ,  Lin Xie  2 ,  Yanlong Liu  2 ,  Jian Xiao  1  2 ,  Xiangyang Wang  1
Affiliations
  • 1. Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 2. Molecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 3. The Second School of Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, China.
PMID: 31885823 DOI: 10.1155/2019/8783197
Abstract

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.

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