[Capsaicin Alleviate Myocardial Ischemia Reperfusion Injury Through Attenuating Mitochondrial Oxidative Stress].

Objective: To investigate the role of capsaicin (CAP) in myocardial ischemia reperfusion injury and its underlying mechanisms.

Methods: Twentyfour adult male SD rats were randomized into 4 groups,namely the control group,ischemia reperfusion group,ischemia reperfusion with CAP group,and ischemia reperfusion with CAPZ and CAP group. Isolated rat hearts underwent Langendorff perfusion. Left ventricular enddiastolic pressure (LVEDP) andleft ventricular developed pressure (LVDP) was calculated to evaluate myocardial performance at 30 min of reperfusion.Triphenyltetrazolium chloride staining was used to measure the infarct size of myocardium at 120 min reperfusion. The morphological changes in myocardial fiber was analyzed by HE staining at the end of reperfusion. Lactate dehydrogenase (LDH) content in the coronary flow was determined during the first 5 min reperfusion. The myocardial mitochondria was isolated and extracted for measuring a series of indicators of mitochondrial oxidative stress,including superoxide dismutase (SOD),methane dicarboxylic aldehyde (MDA) at the end of reperfusion. Western blot was used to determine the expression of caspase3 and cytochrome c at 10 min reperfusion.

Results: Compared with the control group,IR group significantly decreased in cardiac function,the level of LVDP and SOD activity and induced an enlarged infarct size ( <0.01),accompanied by the disordered arrangement of myocardial cells,the content of MDA was increased ( <0.01),the content of caspase3 and cytochrome c were also upregulated ( <0.01).10 μmol/L CAP significantly attenuated these effects induced by ischemia reperfusion injury,levels of LVDP and infarct size at the end of reperfusion were significantly improved( <0.01),nevertheless levels of LVEDP and MDA at the end of reperfusion and LDH were down-regulated markedly ( <0.01),the content of caspase-3 and cytochrome c were also decreased ( <0.01).

Conclusion: These results demonstrate that CAP can suppresses cell apoptosis and necrosis,and alleviate heart function and cell survival from ischemia reperfusion injury through attenuating mitochondrial oxidative stress.