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河可以通过AMPK-SIRT3正反循环介导的线粒体自来缓解骨关节炎

Peng-Bo Shi¹, Meng-Meng Du², Peng Yu²

¹Department of Orthopedics, The First Afliated Hospital of Henan University of Chinese Medicine, Zhengzhou, 450000, China; Engineering Research Center For Traditional Chinese Orthopedics Characteristic Technology and Equipment by Henan Province, Zhengzhou, 450000, China.

Journal of ethnopharmacology

|January 2, 2025

概括

河 (YHD) 通过减少状细胞亡和炎症来保护骨关节炎 (OA). 它的机制涉及激活髓和AMPK-SIRT3通路,为OA提供潜在的治疗益处.

科学领域:

传统中国医药传统中国医药
药理学药理学是指药理学的学科.
骨关节炎研究骨关节炎研究

背景情况:

阳河 (YHD) 是一种传统的中医药,已知对骨关节炎 (OA) 有效.
了解OA中YHD的分子机制对于其治疗应用至关重要.

研究的目的:

阐明河 (YHD) 在治疗关节炎 (OA) 中的潜在机制.
研究YHD对状细胞亡,线粒细胞亡和相关信号通路的影响.

主要方法:

超高性能液态染色体质谱法 (UHPLC-MS) 确定了YHD的组件.
一种体内骨关节炎小鼠模型用YHD进行治疗,而体内研究使用了YHD含有的血清,用于用脂多糖 (LPS) 刺激的小鼠冠状细胞.
用形态观测,流细胞计和蛋白质水平检测来评估保护作用.

主要成果:

在体内,YHD降低了冠状细胞亡和关节炎症,促进了线粒细胞和增加了p-AMPK,SIRT3,PINK1,帕金和LC3II/I的水平.
在体外,含有YHD的血清降低了氏体亡,减少了线粒体活性氧物种 (ROS),并增强了线粒体膜潜力.
关键蛋白质包括p-AMPK,SIRT3,PINK1,帕金和LC3II/I在体外上调.

结论:

河 (YHD) 证明了对骨关节炎中亡的冠状动脉保护作用.
YHD的治疗机制可能涉及调节AMPK-SIRT3正反循环.
激活PINK1/Parkin介导的线粒是YHD在OA中发挥保护作用的关键途径.

关键词:

在AMPK-SIRT3反循环中.冠状细胞 (chondrocytes) 是一种细胞.线粒细胞衰变 (mitophagy) 是一种神经衰变的过程.骨关节炎是一种骨关节炎.河制剂河制剂

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