RESUMO
In the paper, we observed the effect of ellagic acid (EA) on myocardial morphology and cardiac function and explored the mechanism of miR-140-3p-mediated EA in ventricular remodeling. The experimental animals were divided into 3 groups: control group, AMI group, AMI+EA group. Intragastric administration for 4 weeks was initiated on the first day after surgery in rats. Rodent echocardiography was used to measure heart size and cardiac function. The level of fibrosis was observed by Masson staining. The number of cell apoptosis was detected by TUNEL method. The expression of miR-140-3p and MKK6 was measured by qRT-PCR and Western blot, respectively. The results showed that EA could effectively improve the left ventricular function of AMI rats, reduce fibrosis area and infarct area. Moreover, EA significantly increased the expression of miR-140-3p and inhibited the expression of MKK6. However, miR-140-3p inhibitor up-regulated MKK6 expression, and miR-140-3p overexpression reversed the expression. In addition, EA could inhibit cell apoptosis, while miR-140-3p inhibitor increased cell apoptosis. After transfection with si-MKK6, the level of cell apoptosis was significantly decreased. These results indicated that EA improved ventricular remodeling after myocardial infarction by up-regulating miR-140-3p expression and inhibiting MKK6 expression.