Gene transfer of heat-shock protein 20 protects against ischemia/reperfusion injury in rat hearts

<正> Aim: To explore whether overexpression of HSP20 in the myocardium could protect against ischemia/reperfusion injury in rats. Methods: Rat hearts were injected with vector, recombinant adenovirus encoding green fluorescent protein（Ad.GFP） or recombinant adenovirus encoding wild-type HSP20 （Ad.HSP20） in the left ventricle. Four days later, hearts were removed and expression of HSP20was measured in the left ventricle. Subsets of animals in the vector-, Ad.GFP-, andAd.HSP20-treated groups were subjected to 20-rain ischemia and 120-rainreperfusion. Myocardial injury was evaluated by infarct size and level of serumcardiac troponin T and creatine phosphokinase. Apoptosis of cardiomyocyteswas determined by TUNEL staining. Cardiac function was evaluated by hemodyamic indexes. Results: Infarct size and serum cardiac troponin T and creatinephosphokinase levels were significantly reduced in Ad.HSP20-treated hearts compared with vector-and Ad.GFP-treated hearts. The ratio of TUNEL-positivecardiomyocytes to total number of cardiomyocytes in the Ad.HSP20 group wassignificantly reduced as compared with the vector and Ad.GFP groups. Left ventricular end systolic pressure, and maximal rate of pressure increase (+dp/dtmax)and decrease (-dp/dtmin) values were increased significantly, while left ventricularend diastolic pressure was decreased significantly in Ad.HSP20-treated heartscompared with vector- and Ad.GFP-treated hearts. Conclusion: These data indicate that the cardioprotective effects of HSP20 may contribute to the reduction ofmyocardial necrosis and apoptosis in ischemia/reperfusion injury in rats.