The effect of neuregulin-1 on myocardial ischemia reperfusion injury in rats

Abstract

Objective To investigate the effect and mechanism of neuregulin-1 (NRG-1) on myocardial ischemia reperfusion injury in rats. Methods The model of myocardial ischemia and reperfusion in rats were randomly divided into the model group and the NGR-1 group. At the same time, set up the sham operation group, and the left anterior descending artery of the sham operation group was not ligation. NRG-1 group rats were injected with NRG-1 before modeling. Three phenyl tetrazolium chloride (TTC) method was used to detect the myocardial infarct size in rat heart. Isolated rat myocardial cells, flow cytometry was used to detect cell apoptosis. Detection of B cell lymphoma/leukemia 2 (bcl-2), bcl-2 related X protein (bax), signal transduction and transcription factor 3 (STAT3), phosphorylated STAT3 (p-STAT3) protein and reactive oxygen species (ROS) level, SOD activity and malondialdehyde (MDA) content in cardiac tissue. Results The myocardial infarction area of model group was higher than that of sham operation group (P=0.000), and the infarct size of NRG-1 group was lower than that of model group (P=0.000). In model group, myocardial apoptosis was significantly more than that in sham operation group (P=0.000), the rate of myocardial apoptosis in NRG-1 group was significantly lower than that in model group (P=0.000). The myocardial tissue of bcl-2 and p-STAT3 levels in the model rats were significantly lower than the sham operation group (P=0.000), bcl-2 and p-STAT3 level of myocardial tissue in NRG-1 rats was higher than in the model group (P=0.000). The level of bax in myocardial tissue of rats in the model group was higher than in the sham operation group (P=0.000), the bax level of myocardial tissue in NRG-1 rats was lower than the model group (P=0.000). The levels of ROS and MDA in the model group were significantly higher than those in the sham operation group (P=0.000). The levels of ROS and MDA in NRG-1 group were significantly lower than those in model group (P=0.000). In model group, the activity of SOD was significantly lower than that of sham operation group (P=0.000). The activity of SOD in NRG-1 group was significantly higher than that in model group (P=0.000). Conclusion NRG-1 can effectively improve the myocardial ischemia reperfusion injury, and the mechanism of action is related to the regulation of myocardial apoptosis and antioxidation. Key words: Myocardial ischemia reperfusion; Neuregulin-1; Apoptosis; Oxygen free radical