Autoantibodies against β3-adrenoceptor reduce the susceptibility to myocardial ischemic/reperfusion injury of heart failure rats. (12th October 2011) - Xiurui, Ma
Abstract : Objective: Choosing chronic heart failure rats as starting point, to observe whether Autoantibodies against β3 -adrenoceptor (β3 AA) can reduce the susceptibility to myocardial ischemic/reperfusion injury of heart failure rats, then to study whether β3 AA have cardio protective effect to the heart failure rats. Methods: β3 AA was produced through actively immunised method; The level of β3 AA in the sera was detected by ELISA, β3 AA positive/negative IgG were purified by Mab Trap Kit (Amersham, USA), BCA Protein Assay kit (Pierce, USA) was used for protein quantitation, the purities of extractions were assessed by conventional SDS-PAGE; Aortic banding surgery was used to prepare the heart failure model, Ligating the left anterior descending coronary artery for 30 min, then loose the ligature for reperfusion 3 h to make the myocardial ischemia/reperfusion injury, TTC coloration is used to detect the myocardial infarct sise, caspase 3 ability assay and TdT-mediated dUTP nick end labelling were used to detect the apoptosis. Results: After β3 AA was administrated to the rats, the myocardial infarct size induced by ischemia/reperfusion injury was smaller than that in the control group (48.81±6.45% vs 60.25±2.52%, p<0.05); after the heart failure rats undergo the myocardial ischemia/reperfusion injury, the TUNEL-positive cells and the apoptosis index both were significantly lower in β3 AA positive group than in β3 AA negative group (24.33±1.82% vs 31.24±1.31%, p<0.01); moreover compared with the β3 AA negative group, the caspase-3 activity in myocardiocytes was also lower in β3 AA positive group (1941±150.0 vs 1485±89.39, p<0.01). Conclusion: β3 AA can decrease the myocardial infarct size and cardiomyocyte apoptosis induced by ischemia/reperfusion injury in heart failure rats, so β3 AA reduce the susceptibility to myocardial ischemic/reperfusion injury of heart failure rats.