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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Astragaloside IV protects cardiomyocytes from anoxia/reoxygenation injury by upregulating the expression of Hes1 protein
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Astragaloside IV protects cardiomyocytes from anoxia/reoxygenation injury by upregulating the expression of Hes1 protein

机译：黄芪甲苷IV通过上调Hes1蛋白的表达保护心肌细胞免受缺氧/复氧损伤

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摘要

Astragaloside IV (ASI), a traditional Chinese medicine, is a main active ingredient of Astragalus membranaceus. Many clinical studies have found that ASI protects cardiomyocytes in cardiovascular diseases, but the underlying mechanisms remain obscure. The aim of this study was to investigate the molecular mechanisms responsible for the protective effects of ASI in cardiomyocytes from anoxia/reoxygenation (A/R) injury. According to the previous studies, we hypothesized that the cardioprotective effects of ASI against A/R injury might be associated with Notch1/Hes1 signaling pathway. In this study, neonatal rat primary cardiomyocytes were preconditioned with ASI prior to A/R injury. Our results showed that ASI effectively increased the cell viability, decreased the content of MDA, decreased the activities of CPK and LDH, increased the activities of GSH-Px and SOD, and reduced the reactive oxygen species (ROS) generation and the loss of mitochondrial membrane potential (Delta Psi(m)). ASI inhibited the mitochondrial permeability transition pore (mPTP) opening and activation of caspase-3, and finally decreased the cell apoptosis in cardiomyocytes. Furthermore, ASI upregulated Hes1 protein expression. However, pretreatment with DAPT, a Notch1 inhibitor, effectively attenuated the cardioprotective effects of ASI against A/R injury, except MDA, SOD, GSH-Px, and the ROS generation. Taken together, we demonstrated that ASI could protect against A/R injury via the Notch1/Hes1 signaling pathway.
机译：黄芪甲苷IV（ASI）是中药，是黄芪的主要活性成分。许多临床研究发现，ASI可保护心血管疾病中的心肌细胞，但其潜在机制仍不清楚。这项研究的目的是调查负责ASI对缺氧/复氧（A / R）损伤的心肌细胞保护作用的分子机制。根据以前的研究，我们假设ASI对A / R损伤的心脏保护作用可能与Notch1 / Hes1信号通路有关。在这项研究中，新生大鼠原代心肌细胞在A / R损伤之前用ASI预处理。我们的结果表明，ASI有效地提高了细胞活力，降低了MDA的含量，降低了CPK和LDH的活性，增加了GSH-Px和SOD的活性，并减少了活性氧（ROS）的产生和线粒体的损​​失膜电位（Delta Psi（m））。 ASI抑制线粒体通透性过渡孔（mPTP）的开放和caspase-3的激活，并最终减少了心肌细胞的细胞凋亡。此外，ASI上调Hes1蛋白表达。但是，用Notch1抑制剂DAPT预处理可有效减弱ASI对A / R损伤的心脏保护作用，除了MDA，SOD，GSH-Px和ROS产生。综上所述，我们证明了ASI可以通过Notch1 / Hes1信号通路来预防A / R损伤。

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