Kaempferol protects cardiomyocytes against anoxia/reoxygenation injury via mitochondrial pathway mediated by SIRT1

心肌保护 细胞凋亡 细胞色素c 活性氧 再灌注损伤 线粒体 细胞生物学 活力测定 化学 MPTP公司 生物化学 生物 缺血 医学 内科学 内分泌学 多巴胺能 多巴胺
作者
Zhen Guo,Zhangping Liao,Liqing Huang,Dan Liu,Dong Yin,Ming He
出处
期刊:European Journal of Pharmacology [Elsevier]
卷期号:761: 245-253 被引量:83
标识
DOI:10.1016/j.ejphar.2015.05.056
摘要

Mitochondria-mediated apoptosis is a critical mechanism of anoxia/ reoxygenation (A/R)-induced injury in cardiomyocytes. Kaempferol (Kae) is a natural polyphenol and a type of flavonoid, which has been demonstrated to protect myocardium against ischemia/reperfusion (I/R) injury. However, the mechanism is still not fully elucidated. We hypothesize that Kae may improve the mitochondrial function during I/R injury via a potential signal pathway. In this study, an in vitro I/R model was replicated on neonatal rat primary cardiomyocytes by A/R treatment. Cell viability was monitored by the 3-(4,5-dimethylthiazol- 2-yl)-5-(3- carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H-tetrazolium (MTS) assay. The levels of intracellular reactive oxygen species, mitochondrial membrane potential (Δψm) and apoptosis were determined by flow cytometry. Protein expression was detected by Western Blotting. mPTP opening and the activity of caspase-3 were measured by colorimetric method. The results showed that Kae effectively enhanced the cell viability and decreased the LDH release in cardiomyocytes subjected to A/R injury. Kae reduced the A/R-induced reactive oxygen species generation, the loss of Δψm, and the release of cytochrome c from mitochondria into cytosol. Kae inhibited the A/R-stimulated mPTP opening and activation of caspase-3, and ultimate decrease in cardiomyocytes apoptosis. Furthermore, we found Kae up-regulated Human Silent Information Regulator Type 1 (SIRT1) expression, indicating SIRT1 signal pathway likely involved the cardioprotection of Kae. Sirtinol, a SIRT1 inhibitor, abolished the protective effect of Kae in cardiomyocytes subjected to A/R. Additionally, Kae significantly increased the expression of Bcl-2. Thus, we firstly demonstrate that Kae protects cardiomyocytes against A/R injury through mitochondrial pathway mediated by SIRT1.
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