ArticleAmerican journal of translational research2026
Salvianolic acid B protects cardiac function via β3-AR/miRNA-1 axis-mediated cardiomyocyte proliferation in myocardial infarction rats.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo investigate whether Salvianolic Acid B (SAB) promotes cardiomyocyte proliferation by activating the β3-adrenergic receptor (β3-AR)/microRNA-1 (miR-1) axis, thereby improving cardiac function following myocardial infarction.
methodsA rat model of myocardial infarction was established using left anterior descending artery ligation. Rats were randomly divided into 7 groups: sham surgery group, MI group, MI + SAB group, MI + β3-AR agonist group, MI + SAB + β3-AR antagonist group, MI + SAB + miR-1 mimic group, and MI + negative control RNA group. Echocardiography was used to assess cardiac function; TTC, Masson's, and H&E staining were used to evaluate infarct, fibrosis, and necrosis areas; and Ki67 immunohistochemistry was used to detect cardiomyocyte proliferation. In vitro experiments utilized a hypoxia/reoxygenation (H/R) model in neonatal rat cardiomyocytes, with interventions including SAB, β3-AR modulators, or miR-1 mimics/inhibitors. Cell proliferation was assessed using EdU staining, while molecular mechanisms were examined via qPCR, Western blot, and dual-luciferase reporter assays.
resultsSAB treatment significantly improved left ventricular ejection fraction (LVEF) and fractional shortening (LVFS) in MI rats, reduced infarct and fibrosis areas, and increased the proportion of Ki67-positive cardiomyocytes. Mechanistically, SAB upregulated β3-AR expression, downregulated miR-1 expression, and increased the protein levels of miR-1 target genes CDK4 and Cyclin D1. β3-AR antagonists or miR-1 mimic could block the aforementioned protective effects of SAB. In vitro experiments confirmed that SAB promoted EdU incorporation in H/R-injured cardiomyocytes, downregulated miR-1, and upregulated Cyclin D1; β3-AR antagonist or miR-1 mimic could eliminate these effects. Dual luciferase reporter assays confirmed that miR-1 directly targets the 3'UTR of CDK4.
conclusionSAB improves cardiac function after myocardial infarction by activating the β3-AR/miR-1 axis, thereby lifting miR-1's inhibition of CDK4 and Cyclin D1 and promoting cardiomyocyte proliferation. This study reveals a novel mechanism underlying the cardioprotective effects of SAB and identifies the β3-AR/miR-1 axis as a potential therapeutic target for cardiac regeneration following myocardial infarction.
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