ArticleCoronary artery disease2026
Sophoricoside enhances reparative macrophage polarization to promote cardiac repair postmyocardial infarction through PPAR-γ.
Article in Coronary artery disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The context-dependent roles of PPAR-γ in adipocyte differentiation and obesity: a master regulator with dual functions.Frontiers in nutrition · 2026Review
- Research progress on targeting autophagy pathways with medicinal plants and their active metabolites for the treatment of heart failure.Frontiers in pharmacology · 2026Review
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Authors and funding
2 authors.
Funding
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Abstract
backgroundMyocardial infarction (MI) represents a significant cardiovascular condition that endangers human health. This research aimed to explore the therapeutic effectiveness of sophoricoside (Sop) using a mouse model of MI.
methodsTo conduct this investigation, a mice model of MI was utilized, and Sop was delivered through oral administration via gavage. The area of MI in mice was assessed by Masson trichrome staining. Cardiac systolic function and left ventricular dilatation were measured by cardiac ultrasound. Picrosirius red staining and Masson's trichrome staining were performed to detect the collagen deposition and fibrosis. The expressions of reparative macrophage-associated markers were measured by quantitative real-time PCR. Western blotting was utilized to sense expression of lysyl oxidase (LOX), peroxisome proliferator-activated receptor γ (PPAR-γ), and collagen 1. Flow cytometry was performed to detect the number of macrophages. The Cell Counting Kit-8 assay was performed to detect Sop's cytotoxicity. The M2 polarization and efferocytosis in mice model of MI was verified by immunofluorescence assay.
resultsSop significantly reduced myocardial infarct size. Cardiac ultrasound evaluation further showed that Sop was effective in improving cardiac systolic dysfunction and left ventricular dilatation. In addition, Sop significantly promoted efferocytosis and reparative M2 macrophage polarization and inhibited glycolytic metabolic pathways, thereby promoting cardiac tissue repair. It was further found that Sop could obviously promote expression of PPAR-γ in the nucleus. GW9662 partially reversed the improvement of Sop on cardiac repair and reparative macrophage polarization in MI mice.
conclusionIn summary, this study elucidates that Sop enhances reparative macrophage polarization to promote cardiac repair post-MI through PPAR-γ.
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