Isoquercetin ameliorated hypoxia/reoxygenation-induced H9C2 cardiomyocyte apoptosis via a mitochondrial-dependent pathway

被引：33
作者：
Cao, Heng [1 ]
Xu, Hao [1 ]
Zhu, Guoqing [2 ]
Liu, Shaowen [1 ]
机构：
[1] Nanjing Med Univ, Shanghai Gen Hosp, Dept Cardiol, 100 Haining Rd, Shanghai 200080, Peoples R China
[2] Tongji Univ, Sch Med, Shanghai, Peoples R China
来源：
BIOMEDICINE & PHARMACOTHERAPY | 2017年 / 95卷
关键词：
Isoquercetin; Hypoxia/reoxygenation; H9C2; cells; Apoptosis; ROS generation; Mitochondrial pathway; ISCHEMIA-REPERFUSION INJURY; CELL-DEATH; ACTIVATION; ISOQUERCITRIN; PROTECTS;
D O I：
10.1016/j.biopha.2017.08.128
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Isoquercetin exerts multiple pharmacological effects against various diseases. The present research sought to further investigate the role of isoquercetin in hypoxia/reoxygenation (H/R)-treated cardiomyocytes and its potential mechanism involved. The H/R model in H9C2 cells was established to mimic myocardial I/R injury in vitro. Cell proliferation and apoptosis were tested using MTT assay and Annexin V FITC-PI staining assay, respectively. We found that isoquercetin protected H9C2 cells from H/R-induced injury as the evidences that isoquercetin administration attenuated the effects of H/R treatment on H9C2 cell viability, cell apoptosis and ROS generation after H/R treatment. More importantly, isoquercetin protects mitochondrial function and prevents cytochrome c release in H9C2 cells after I/R injury. In conclusion, these results revealed the potential cardiovascular protective effects of isoquercetin in the treatment of I/R-related myocardial injury.
引用
收藏
页码：938 / 943
页数：6
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