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-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 proteins and 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.

中文翻译：

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厚朴酚通过抑制SIRT1 / AMPK /PGC-1α信号通路减轻IL-1β诱导的软骨细胞功能障碍。

骨关节炎是一种常见的慢性关节疾病，与线粒体功能障碍，损伤和软骨细胞合成缺陷有关。厚朴酚是从厚朴中提取的木质素，具有抗氧化和抗炎功能。本研究旨在研究厚朴酚对人原代软骨细胞线粒体功能异常，氧化应激和炎症的作用。IL-1β刺激软骨细胞以模仿骨关节炎的发病机理。细胞存活力通过3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑鎓溴化物分析来分析，并使用ELISA检查炎性细胞因子IL-8的浓度。Western blot检测SIRT1 / pAMPK /PGC-1α，代谢相关蛋白和Cox2的蛋白表达。线粒体功能，活性氧浓度，使用商业试剂盒分别分析超氧化物歧化酶活性和NF-κB活性。我们证明厚朴酚增加了人类软骨细胞中SIRT1 / AMPK /PGC-1α的表达。厚朴酚可通过SIRT1 / AMPK /PGC-1α信号通路减轻人软骨细胞中IL-1β诱导的线粒体功能障碍和氧化应激。此外，厚朴酚通过SIRT1 / AMPK /PGC-1α信号通路维持细胞外基质平衡的合成代谢和分解代谢。此外，厚朴酚减轻了IL-1β诱导的人软骨细胞炎症。厚朴酚通过抑制SIRT1 / AMPK /PGC-1α信号通路减轻IL-1β诱导的软骨细胞功能障碍，为人类骨关节炎提供了潜在的新治疗策略。我们证明厚朴酚增加了人类软骨细胞中SIRT1 / AMPK /PGC-1α的表达。厚朴酚可通过SIRT1 / AMPK /PGC-1α信号通路减轻人软骨细胞中IL-1β诱导的线粒体功能障碍和氧化应激。此外，厚朴酚通过SIRT1 / AMPK /PGC-1α信号通路维持细胞外基质平衡的合成代谢和分解代谢。此外，厚朴酚减轻了IL-1β诱导的人软骨细胞炎症。厚朴酚通过抑制SIRT1 / AMPK /PGC-1α信号通路减轻IL-1β诱导的软骨细胞功能障碍，为人类骨关节炎提供了潜在的新治疗策略。我们证明厚朴酚增加了人类软骨细胞中SIRT1 / AMPK /PGC-1α的表达。厚朴酚可通过SIRT1 / AMPK /PGC-1α信号通路减轻人软骨细胞中IL-1β诱导的线粒体功能障碍和氧化应激。此外，厚朴酚通过SIRT1 / AMPK /PGC-1α信号通路维持细胞外基质平衡的合成代谢和分解代谢。此外，厚朴酚减轻了IL-1β诱导的人软骨细胞炎症。厚朴酚通过抑制SIRT1 / AMPK /PGC-1α信号通路减轻IL-1β诱导的软骨细胞功能障碍，为人类骨关节炎提供了潜在的新治疗策略。厚朴酚可通过SIRT1 / AMPK /PGC-1α信号通路减轻人软骨细胞中IL-1β诱导的线粒体功能障碍和氧化应激。此外，厚朴酚通过SIRT1 / AMPK /PGC-1α信号通路维持细胞外基质平衡的合成代谢和分解代谢。此外，厚朴酚减轻了IL-1β诱导的人软骨细胞炎症。厚朴酚通过抑制SIRT1 / AMPK /PGC-1α信号通路减轻IL-1β诱导的软骨细胞功能障碍，为人类骨关节炎提供了潜在的新治疗策略。厚朴酚可通过SIRT1 / AMPK /PGC-1α信号通路减轻人软骨细胞中IL-1β诱导的线粒体功能障碍和氧化应激。此外，厚朴酚通过SIRT1 / AMPK /PGC-1α信号通路维持细胞外基质平衡的合成代谢和分解代谢。此外，厚朴酚减轻了IL-1β诱导的人软骨细胞炎症。厚朴酚通过抑制SIRT1 / AMPK /PGC-1α信号通路减轻IL-1β诱导的软骨细胞功能障碍，为人类骨关节炎提供了潜在的新治疗策略。