Cardioprotective Role And Its Possible Mechanism Of The Hangover Medicine On Myocardial Ischemia-reperfusion Injury In Rats

Background Myocardial ischemia-reperfusion Injury (MIRI) become the main problems of ischemic cardiomyopathy after recanalization, its occurrence and development seriously affect the prognosis of patients. Many molecular mechanism and signal pathway involved in myocardial ischemia-reperfusion injury. Oxygen free radical, calcium overload, cell apoptosis caused by variety of factors, mitochondrial membrane permeability transition pore opening and so on are involved in myocardial ischemia-reperfusion injury. And endoplasmic reticulum stress can lead to cell apoptosis, which makes the decrease in the number of live cells. Many experiments confirmed that the key enzyme of aldehyde metabolism, aldehyde dehydrogenase2(ALDH2), can play a protective role through various channels. Hangover medicine can influence ALDH2and play a protective role in development of heart failure, but views at home and abroad have not collaboration for reports of acute myocardial ischemia-reperfusion injury.Objective To investigate whether hangover medicine plays cardioprotective role in the rat model of myocardial ischemia-reperfusion injury, and to reveal the possible mechanism whether has to do with supressing endoplasmic reticulum stress responsive via on activity ALDH2. Convenient to promote the clinical treatment of myocardial ischemia-reperfusion injury to provide theoretical basis and treatment ideas.Methods200～25()g Sprague-Dawley rats were divided into3groups randomly, before myocardial ischemia and reperfusion procedure, saline (n=6), hangover medicine (n=6) or hangover medicine+cyanamide were given respectively by oral gavage and intraperitoneal injection. Calculated risk area ratio and infarction ratio by computer image analysis software. Risk area ratio=Risk area (Red ischemia area+White infarction area) /Left ventricular areax100%; Infarction ratio=White infarction area/Risk area (Red ischemia area+White infarction area)×100%. Myocardial infarction ratio was calculated by Evans blue and triphenyltetrazolium chloride (TTC) staining, and myocardial apoptosis was evaluated by TUNEL assay. Expression of endoplasmic-reticulum-stress-related proteins (Grp78,Chop) and apoptosis-related protein (Caspase12) were quantified by western-blot.Results The model were built successfully and its stability is high. The infarction size was significantly reduced by the treatment of hangover medicine (hangover medicine group vs. saline group,35.59±5.77%vs.57.72±6.52%, P<0.01). However, when the hangover medicine was blocked,the protection was diminished (hangover medicine group vs. hangover medicine and cyanamide group,35.59±5.77%vs.46.83±5.96%, P<0.01) Myocardial apoptosis and the levels of Grp78, Chop, Caspase12were not significantly different between the three groups (P>0.05).Conclusion In the early phase of myocardial ischemia and reperfusion injury, hangover medicine provides myocardial protection, which can be blocked by ALDH2inhibitor. This influence may not be implicated through ALDH2initiated endoplasmic reticulum stress...