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山茱萸新苷 C 通过调节线粒体功能保护 H9c2 心肌细胞免受氧化应激。

Araloside C protects H9c2 cardiomyoblasts against oxidative stress via the modulation of mitochondrial function.

机构信息

Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100193, PR China.

Harbin University of Commerce, Harbin, 150076, Heilongjiang, PR China.

出版信息

Biomed Pharmacother. 2019 Sep;117:109143. doi: 10.1016/j.biopha.2019.109143. Epub 2019 Jul 8.

DOI:10.1016/j.biopha.2019.109143
PMID:31387189
Abstract

Araloside C (AsC) has potential cardioprotective properties. However, the underlying mechanism of AsC-mediated cardioprotection, especially the role of mitochondrial function, remains largely unknown. Here, we used H9c2 cardiomyocytes to study the cardioprotective mechanisms of AsC through HO-induced oxidative stress. Cell viability, lactate dehydrogenase release, mitochondrial functions and bioenergetics were evaluated. Western blot analysis was used to measure the protein expression levels of apoptosis and the phosphorylation of AMP-activated protein kinase (AMPK). Results revealed that AsC increased cell viability, improved mitochondrial membrane potential disruption, decreased mitochondrial reactive oxygen species level, elevated cellular ATP levels and alleviated impaired mitochondrial respiration in HO-induced H9c2 cardiomyoblasts injury. Furthermore, AsC modulated apoptosis-associated protein expression and AMPK pathway in H9c2 cells under oxidative stress. In conclusion, AsC potentially protects H9c2 cardiomyoblasts against oxidative stress by regulating mitochondrial function and AMPK activation. AsC may be an effective therapeutic agent for the prevention of oxidative stress in cardiac injury.

摘要

梓醇(AsC)具有潜在的心脏保护作用。然而,AsC 介导的心脏保护的潜在机制,特别是线粒体功能的作用,在很大程度上仍不清楚。在这里,我们使用 H9c2 心肌细胞通过 HO 诱导的氧化应激来研究 AsC 的心脏保护机制。评估细胞活力、乳酸脱氢酶释放、线粒体功能和生物能量。使用 Western blot 分析来测量细胞凋亡和 AMP 激活蛋白激酶(AMPK)磷酸化的蛋白表达水平。结果表明,AsC 增加了细胞活力,改善了线粒体膜电位破坏,降低了线粒体活性氧水平,提高了细胞内 ATP 水平,并减轻了 HO 诱导的 H9c2 成肌细胞损伤中受损的线粒体呼吸作用。此外,AsC 在氧化应激下调节 H9c2 细胞中与细胞凋亡相关的蛋白表达和 AMPK 途径。总之,AsC 通过调节线粒体功能和 AMPK 激活,可能对 H9c2 心肌细胞的氧化应激具有保护作用。AsC 可能是预防心脏损伤中氧化应激的有效治疗剂。

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