Effect of ginsenoside Rb3 on the expression of VE-cadherin, NRG-1, ErbB2 and ErbB4 in rats with myocardial infarction by Neuregulin-1/ErbB signaling pathway

Han Ling; Zhang Jingjing; Qin Li

doi:10.3969/j.issn.1674-4055.2019.02.17

Abstract：Objective To observe the effect of ginsenoside Rb3 on the expression of VE-cadherin, NRG-1, ErbB2 and ErbB4 in rats with myocardial infarction by Neuregulin-1/ErbB signaling pathway. Methods 60 rats were randomly divided into Sham group, Model group, G-Rb3-L group (10 mg/kg), G-Rb3-M group (20 mg/kg), G-Rb3-H group (40 mg/kg ) and positive drug group (Diltiazem 20mg/kg), with 10 rats in each group. After modeling, the G-Rb3-L group, the G-Rb3-M group, the G-Rb3-H group and the positive drug group were given relative drugs, and the Model group and the Sham group were given an equal volume of physiological saline. The pathological changes of myocardial tissue and the degree of myocardial fibrosis were observed by HE and Masson staining. The levels of VE-cadherin in plasma were detected by ELISA. The expressions of NRG-1, ErbB2 and ErbB4 in myocardial tissue were detected by Western blotting. Results Compared with the Sham group, the myocardial infiltration and myocardial fibrosis were severe in the model group, myocardial infarct size, VE-cadherin protein were significantly increased (P<0.05), and the expression levels of NRG-1, ErbB2, and ErbB4 proteins were significantly reduced (P<0.05). Compared with the Model group, after intervention with ginsenoside Rb3, the cardiomyocyte inflammatory infiltration and myocardial fibrosis were reduced, myocardial infarct size and VE-cadherin protein expression were significantly reduced (P<0.05). NRG-1, ErbB2 and ErbB4 protein expression was significantly increased (P<0.05). Conclusion Ginsenoside Rb3 through Neuregulin-1/ErbB signaling pathway can effectively reduce the myocardial inflammation and myocardial fibrosis in myocardial infarction rats, and reduce myocardial infarct size and myocardial injury.