Research Paper|Volume 15, Issue 10|pp 4084—4095

Xuesaitong promotes myocardial angiogenesis in myocardial infarction mice by inhibiting MiR-3158-3p targeting Nur77

Jiangquan Liao¹, Mingjing Shao¹, Yan Wang¹, Peng Yang¹, Dongliang Fu¹, Mengru Liu¹, Tong Gao², Kangkang Wei³, Xianlun Li¹, Jinhang Du¹

¹National Integrated Traditional and Western Medicine Center for Cardiovascular Disease, China–Japan Friendship Hospital, Beijing, China
²Department of Cardiology, Beijing Tsinghua Changgung Hospital, Medical Center, Tsinghua University, Beijing, China
³Graduate School, Beijing University of Chinese Medicine, Beijing, China

Received: January 26, 2022Accepted: March 21, 2023Published: April 20, 2023

https://doi.org/10.18632/aging.204671

Copyright: © 2023 Liao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.