Wei Xiaoyi, Zheng Yalin, Ai Yanke, Li Buman
Beijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, Beijing 100069, China.
Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing 100700, China.
Evid Based Complement Alternat Med. 2022 Jan 11;2022:7864308. doi: 10.1155/2022/7864308. eCollection 2022.
This study aimed to observe the regulatory effects of astragaloside IV (AS-IV) on hyperglycemia-induced mitochondrial damage and mitophagy in Schwann cells and to provide references for clinical trials on AS-IV in the treatment of diabetic peripheral neuropathy.
Schwann cells were grown in a high-glucose medium to construct an autophagy model; the cells were then treated with AS-IV and N-acetylcysteine (control) to observe the regulatory effects of AS-IV on oxidative stress and mitophagy.
AS-IV exhibited antioxidant activity and inhibited the overactivation of autophagy in Schwann cells, significantly reducing the level of reactive oxygen species and downregulating the expression of autophagy-related proteins (LC3, PINK, and Parkin) under hyperglycemic conditions, thereby exerting a protective effect on mitochondrial morphology and membrane potential.
AS-IV can maintain the mitochondrial function of Schwann cells under hyperglycemic conditions by effectively alleviating oxidative stress and overactivation of mitophagy. The evidence from this study supports an AS-IV-based therapeutic strategy against diabetic peripheral neuropathy.
本研究旨在观察黄芪甲苷IV（AS-IV）对高血糖诱导的施万细胞线粒体损伤和线粒体自噬的调节作用，为AS-IV治疗糖尿病周围神经病变的临床试验提供参考。
将施万细胞培养于高糖培养基中构建自噬模型；然后用AS-IV和N-乙酰半胱氨酸（对照）处理细胞，观察AS-IV对氧化应激和线粒体自噬的调节作用。
AS-IV具有抗氧化活性，可抑制施万细胞自噬的过度激活，显著降低高血糖条件下活性氧水平，下调自噬相关蛋白（LC3、PINK和Parkin）的表达，从而对线粒体形态和膜电位发挥保护作用。
AS-IV可通过有效减轻氧化应激和线粒体自噬的过度激活，维持高血糖条件下施万细胞的线粒体功能。本研究证据支持基于AS-IV的糖尿病周围神经病变治疗策略。
