Magnolol Alleviates IL-1β-Induced Dysfunction of Chondrocytes Through Repression of SIRT1/AMPK/PGC-1α Signaling Pathway

Osteoarthritis is a common chronic joint disease related with mitochondrial dysfunction, damage, and synthetic defects in chondrocytes. Magnolol is a lignin extracted from Magnolia officinalis with antioxidant and anti-inflammation functions. This study aims to investigate the function of magnolol on mitochondrial dysfunction, oxidative stress, and inflammation in human primary chondrocytes. Chondrocytes were stimulated with IL-1 beta to mimic the pathogenesis of osteoarthritis. Cell viability was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and ELISA was employed to examine the concentration of inflammatory cytokine IL-8. Protein expression of SIRT1/pAMPK/PGC-1 alpha, metabolism-related proteins and Cox2 were examined by Western blot. Mitochondrial function, reactive oxygen species concentration, superoxide dismutase activity, and NF-kappa B activity were analyzed using commercial kit, respectively. We demonstrated that magnolol increased SIRT1/AMPK/PGC-1 alpha expression in human chondrocytes. Magnolol could alleviate IL-1 beta-induced mitochondrial dysfunction and oxidative stress through SIRT1/AMPK/PGC-1 alpha signaling pathway in human chondrocytes. In addition, magnolol maintained the anabolism and catabolism of extracellular matrix balance by SIRT1/AMPK/PGC-1 alpha signaling pathway. Furthermore, magnolol alleviated IL-1 beta-induced inflammation in human chondrocytes. Magnolol alleviates IL-1 beta-induced dysfunction of chondrocytes through repressing SIRT1/AMPK/PGC-1 alpha signaling pathway, which provides a potential new therapeutic strategy for human osteoarthritis.