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Abstract Title:

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

Abstract Source:

J Interferon Cytokine Res. 2020 Jan 9. Epub 2020 Jan 9. PMID: 31916911

Abstract Author(s):

Zili Liu, Hao Zhang, Honglin Wang, Longyu Wei, Lei Niu

Article Affiliation:

Zili Liu

Abstract:

Osteoarthritis is a common chronic joint disease related with mitochondrial dysfunction, damage, and synthetic defects in chondrocytes. Magnolol is a lignin extracted fromwith 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-1β 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-1α, metabolism-related proteinsand Cox2 were examined by Western blot. Mitochondrial function, reactive oxygen species concentration, superoxide dismutase activity, and NF-κB activity were analyzed using commercial kit, respectively. We demonstrated that magnolol increased SIRT1/AMPK/PGC-1α expression in human chondrocytes. Magnolol could alleviate IL-1β-induced mitochondrial dysfunction and oxidative stress through SIRT1/AMPK/PGC-1α signaling pathway in human chondrocytes. In addition, magnolol maintained the anabolism and catabolism of extracellular matrix balance by SIRT1/AMPK/PGC-1α signaling pathway. Furthermore,magnolol alleviated IL-1β-induced inflammation in human chondrocytes. Magnolol alleviates IL-1β-induced dysfunction of chondrocytes through repressing SIRT1/AMPK/PGC-1α signaling pathway, which provides a potential new therapeutic strategy for human osteoarthritis.

Study Type : In Vitro Study

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