Cardiac Shock Wave Treatment Enhances Myocardial Function in Rat Model of Myocardial Infarction by Regulating MAPK Signaling Pathway

Abstract

Background: Cardiac shock wave therapy (CSWT) can inhibit cardiomyocyte apoptosis via several unknown mechanisms. The mitogen-activated protein kinase (MAPK) signaling pathway plays a pivotal role in cardiac and myocardial function by regulating tissue fibrosis and apoptosis. In this study we investigated the potential effects of CSWT on MAPK signaling pathway in the rat model of myocardial infarction (MI). Material and Methods: A total of 32 male Sprague-Dawley (SD) rats were enrolled in this study and MI was induced through coronary artery ligation surgery. In the model group, CSWT was performed in the presence or absence of MAPK inhibitor/activator for 4 weeks, and the therapeutic effect was compared with the model group and control groups. Hematoxylin and eosin (H&E) and Massons trichrome staining were used for histological evaluation. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were used for protein and mRNA expression analysis. Echocardiography was used for cardiac function assessment. Results: H&E staining and Masson staining revealed that MI induction in the model group caused the disruption of myocardial tissues in the infarcted myocardium, and increased the area of collagen staining area (p < 0.05). After CSWT intervention, the damages in the myocardial tissues were ameliorated in the MI model group and the collagen area was considerably reduced (p < 0.05). Protein p38, Extracellular signal-regulated kinase 1 (Erk1) and Erk2 levels were upregulated upon the induction of MI in the model group, CSWT intervention suppressed their overexpression (p < 0.05). The application of MAPK activator abrogated the effect of CSWT intervention in the MI model group (p < 0.05). In the MI model group, the administration of MAPK inhibitor showed similar protective effects as CSWT intervention (p < 0.05). Conclusions: CSWT can promote cardiac function and reduce myocardial fibrosis in the rat model of MI by regulating MAPK signaling pathway.