ArticleBioMed research international2026
Compound Astragalus Oral Liquid Attenuates Ventricular Remodeling in Heart Failure After Myocardial Infarction via the AMPK/TGF-β/Smad Signaling Pathway.
Article in BioMed research international, 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
backgroundVentricular remodeling following acute myocardial infarction (AMI) is a critical cause of heart failure (HF). Compound Astragalus Oral Liquid (CAOL) is a traditional Chinese medicine formulation with anti-inflammatory, antioxidant, and tonifying properties. However, its effects and underlying mechanisms in post-acute myocardial infarction heart failure (AMI-HF) remain unclear.
objectiveTo evaluate the cardioprotective efficacy of CAOL in a rat model of AMI-HF and elucidate the associated molecular mechanisms.
methodsCAOL constituents were identified by UPLC-Q-TOF/MS, and network pharmacology predicted potential targets. A rat model of AMI-induced HF was established by left anterior descending (LAD) coronary ligation. Animals received CAOL at low, medium, and high doses, or perindopril. Cardiac function, histopathology, serum oxidative and inflammatory markers, and myocardial molecular expression were assessed by echocardiography, staining, ELISA, Western blotting, and RT-qPCR.
resultsCAOL treatment improved cardiac performance in a dose-dependent manner, as evidenced by increased LVEF and improvements in LVIDd and LVIDs. Histological analyses demonstrated that CAOL reduced myocardial necrosis, inflammatory cell infiltration, and collagen deposition in a dose-dependent fashion. CAOL also ameliorated serum markers of inflammation and oxidative stress. Mechanistically, CAOL modulated AMPK activity and inhibited TGF-β1/Smad-mediated profibrotic signaling, consistent with its antifibrotic and cytoprotective effects.
conclusionsCAOL ameliorates postinfarction ventricular remodeling and preserves cardiac function in a manner associated with AMPK activation and suppression of TGF-β/Smad-mediated fibrosis. These findings provide experimental evidence supporting CAOL as a potential therapeutic agent for AMI-HF.
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