Objective To explore the effect of platelet derived growth factor (PDGF)/PDGF receptor (PDGFR) pathway on ventricular remodeling after myocardial ischemia-reperfusion injury (MI/RI) and the underlying mechanisms.

Methods A MI/RI mouse model was established, and cardiac function was detected by cardiac ultrasonography, myocardial fibrosis was detected by Masson staining, and the expression of inflammatory factors was determined by quantitative polymerase chain reaction (qPCR) with the intervention of PDGFR phosphorylation inhibitor CP-673, 451. The neonatal rat cardiac fibroblasts (NCF) were isolated. The expression of collagen synthesis genes was analyzed by qPCR, and the phosphorylation level of p38 molecule was analyzed by Western blot.

Results CP-673, 451 can improve the cardiac function index of left ventricular ejection fraction (LVEF), fraction shortening (FS), and left ventricular internal diameter (LVID)after MI/RI in mice (P < 0.05), and reduce the degree of myocardial fibrosis after MI/RI; CP-673, 451 can effectively inhibit the expression of inflammatory factors interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6 mRNA in myocardial infarction after MI/RI (P < 0.05), reduce the increase of Col Ⅰ and Col Ⅲ mRNA caused by PDGF-BB in NCF (P < 0.05), and reduce p38 protein phosphorylation level stimulated by PDGF-BB (P < 0.05).

Conclusion Inhibiting the PDGF/PDGFR pathway during MI/RI can down-regulate the inflammatory response and collagen synthesis in the infarcted myocardium, thereby improving ventricular remodeling, which may play a role via the p38/MAPK signaling pathway.