| ObjectiveTo observe the effects of propylgallate on isoproterenol induced myocardial fibrosis in rats and explore possible mechanism.Methods50 male SD rats,8 weeks old, are randomly divided into 5 groups; normal control group (normal control), model group (model), PrG low dose group (PrG-L), PrG middle dose group (PrG-M) and PrG high dose group (PrG-H),10 of each group. The models of myocardial fibrosis were established by subcutaneous injection of isoproterenol.7 days later, group PrG-L, PrG-M, PrG-H were given PrG 18,36,72mg/kg respectively by intraperitoneal injection for each day, group normal control and model were given equal normal saline by the same way. The spirits, activities, diet and hair are observed during the lab procedure.4 weeks later, the cardiac hemodynamics of rats are determined, calculate heart weight index, observe the pathological changes of myocardial morphology by Masson dyeing and count myocardial CVF, serum TNF-a, IL-1B, IL-6 levels are detected by ELISA kit and the expressions of MMP-9, TIMP-1 in myocardium of rats are tested by western blot.ResultsCompared with group normal control, heart weight index, CVF, TNF-a, IL-1β, IL-6 levels in serum and the expression of MMP-9, TIMP-1 significantly increased in group model (P<0.05). Compared with group model, heart weight index, CVF, TNF-a, IL-1β, IL-6 levels in serum and the expression of MMP-9, TIMP-1 significantly decreased in group PrG-L, PrG-M, PrG-H (P<0.05), and significantly higher than normal control group.ConclusionsPrG can significantly improve cardiac function of rats, reduce collagen fiber content, depress myocardial MMP-9 and TIMP-1 expression and cut the levels TNF-a, IL-1β, IL-6. PrG has the role of prevention and treatment of myocardial fibrosis and the protective mechanism may be related to the inhibition of MMP-9 and TIMP-1 expression in myocardial and lower TNF-α, IL-1β, IL-6 levels. |