Pharmacological postconditioning with tanshinone IIA attenuates myocardial ischemia-reperfusion injury in rats by activating the phosphatidylinositol 3-kinase pathway

被引:72
作者
Yuan, Xun [1 ]
Jing, Songbo [1 ]
Wu, Lingzhen [1 ]
Chen, Lianglong [1 ]
Fang, Jun [1 ]
机构
[1] Fujian Med Univ, Union Hosp, Dept Cardiol, Fujian Inst Coronary Heart Dis, Fuzhou 350001, Fujian, Peoples R China
基金
中国国家自然科学基金;
关键词
tanshinone IIA; postconditioning; myocardial infarction; reperfusion injury; phosphatidylinositol; 3-kinase; mitochondrial permeability transition; MITOCHONDRIAL PERMEABILITY TRANSITION; PORE; PROTECTS; PRETREATMENT; INHIBITION; PI3-KINASE; MECHANISM; APOPTOSIS; HEART;
D O I
10.3892/etm.2014.1820
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
Tanshinone IIA, one of the active ingredients in the Chinese medicine Danshen, is cardioprotective when applied prior to sustained myocardial ischemia. The present study aimed to investigate whether pharmacological postconditioning with tanshinone IIA attenuates myocardial ischemia-reperfusion injury when applied prior to prolonged reperfusion following a sustained ischemia. A total of 88 Sprague-Dawley rats received 30 min myocardial ischemia followed by 5 or 120 min reperfusion. Compared with the ischemia-reperfusion model group, the group that received an intravenous injection of 10 mg/kg tanshinone IIA prior to reperfusion had a reduced myocardial infarct size, higher levels of phospho-Akt and phospho-endothelial nitric oxide synthase and less reduction in the optical density of the mitochondria at 540 nm, indicating that the mitochondrial permeability transition (MPT) was attenuated. The cardioprotective effect conferred by tanshinone IIA was abolished by LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K). These results demonstrate that tanshinone IIA postconditioning protects the myocardium from ischemia-reperfusion injury through the PI3K/Akt pathway, and the MPT may be also involved in this process.
引用
收藏
页码:973 / 977
页数:5
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