This study aims to investigate the regulatory effect of
Xuesaitong (XST) and miR-3158-3p on angiogenesis. All mice were randomly assigned into
Sham group, Model group, XST group, XST + miR-3158-3P-overexpression (
miRNA-OE) group. XST was found to increase the left ventricular anterior wall thickness at end diastole and end systole (LVAWd and LVAWs), left ventricular internal dimension at end diastole and end systole (LVIDd and LVIDs), fractional shortening (FS), and ejection fraction (EF) and decrease the proportion of fibrotic areas in mice. In contrast to those in
Sham group, the
protein expressions of Nur77, p-PI3K, HIF-1α,
VEGFs, COX-2 in the heart tissues of mice in Model group were elevated and further increased after XST treatment in comparison with those in Model group. Nur77-/- mice were utilized. It was found that XST enhanced cell viability through a methyl thiazolyl tetrazolium assay and facilitated angiogenesis in each group, as assessed by a
catheter formation assay. Specifically, XST was shown to promote the formation of blood vessels. Moreover, the
protein expression levels of Associated
proteins in the heart tissues of Nur77-/- mice were dramatically reduced in mice in Model and XST group compared with those in WT mice. Additionally, the above-mentioned
protein expressions in the heart tissues of Nur77-/- mice did not change significantly in mice in Model +
miRNA-OE + XST group compared with those in WT mice, suggesting that miR-3158-3p can specifically inhibit the expression of Nur77. In conclusion, XST inhibits miR-3158-3p targeting Nur77 to facilitate myocardial angiogenesis in mice with
myocardial infarction.