Intermedin1-53 protects cardiac function in rats with septic shock via inhibiting oxidative stress and cardiomyocyte apoptosis.

Abstract

To investigate the protective effect of intermedin1-53 (IMD1-53) on cardiac function in rats with septic shock and its underlying mechanism. Twenty-four male Sprague-Dawley (SD) rats were randomly assigned into three groups, namely the control group (NC group), septic shock group (ET group) and IMD1-53 treatment group (IMD group), with 8 rats in each group. Levels of hemodynamic indicators, blood glucose, lactate acid, CK-MB (creatine kinase-MB) and cTnI (cardiac troponin I) in rats were determined. Cardiac tissues of rats were collected for TUNEL (terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling) staining. Protein levels of caspase-3, caspase-9, Bax, Bcl2, iNOS (inducible nitric oxide synthase) and COX-2 (cyclooxygenase-2) in cardiac tissues were detected by Western blot. Moreover, activities of SOD (superoxide dismutase), CAT (catalase) and MDA (malondialdehyde) in myocardial homogenate were determined, thereby exploring the effect of IMD1-53 on oxidative stress and cardiomyocyte apoptosis in rats with septic shock induced by endotoxin. Lower levels of mean arterial blood pressure (MABP), maximum rate of left ventricular diastolic pressure (+LVdp/dtmax) and left ventricular systolic pressure (LVSP) were observed in ET group than those of NC group (p < 0.05). Levels of lactic acid, blood glucose, CK-MB and cTnI in ET group were remarkably increased than those of NC group (p < 0.05). Moreover, activities of SOD and CAT in myocardial homogenate of ET group were remarkably reduced in comparison with those of NC group (p < 0.05). Protein levels of caspase-3, caspase-9, Bcl-2, Bax, iNOS and COX-2 in ET group were all remarkably elevated than those of NC group (p < 0.05). The above indicators were all significantly improved in IMD group than those of ET group (p < 0 05). IMD1-53 can protect cardiac function in rats with septic shock via inhibiting oxidative stress and cardiomyocyte apoptosis.