Skimmin ameliorates cardiac function via the regulation of M2 macrophages in a myocardial infarction mouse model.

Abstract

Myocardial infarction (MI) is a coronary artery disorder with several complications, such as inflammation, oxidative stress, and cardiac fibrosis. The current study is aimed to explore the protective effect of skimmin (SKI) on impaired heart tissues in MI. A mouse model of MI was induced by ligation of the left anterior descending artery. SKI was intragastric administration for 7days after MI. Masson staining was then conducted to measure the area of fibrosis in the myocardium. The expression levels of collagen I and collagen III were analyzed using Western blot. The levels of glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), and inflammatory factor were also detected. The expression of M1 polarization markers and M2 polarization markers in mice and LPS-induced RAW264.7 cells were detected using RT-qPCR and Western blot, respectively. Finally, the migration and proliferation of vascular smooth muscle cells (VSMCs) in vitro were analyzed using transwell and EDU, respectively. SKI improved cardiac function and cardiac fibrosis in mice with MI. SKI also decreased collagen I and collagen III expression, and inhibited inflammatory factor TNF-α, IL-1β, and IL-6 levels. SKI decreased the levels of MDA and increased the levels of GSH and SOD. Meanwhile, SKI could promote M2 macrophage polarization in vivo and in vitro. SKI could also repress the migration and proliferation of VSMCs. SKI may ameliorate inflammation, oxidative stress, and cardiac fibrosis of MI by promoting M2 polarization.