ArticleInternational journal of applied & basic medical research
Role and Mechanism of Astragalus Monomer Quercetin in Modulating Akt/Bcl-2 Pathway to Improve Ventricular Remodeling in Chronic Heart Failure.
Article in International journal of applied & basic medical research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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3 authors.
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Abstract
Background: Chronic heart failure (CHF), characterized by ventricular remodeling and myocardial fibrosis, remains a major therapeutic challenge. This study investigated the cardioprotective effects of quercetin, an Astragalus-derived bioactive compound, focusing on its modulation of the Akt/Bcl-2 pathway. Methods: This study established both H9C2 cardiomyocyte hypoxia/reoxygenation (H/R) injury models and aortic constriction-induced heart failure (HF) rat models to investigate the cardioprotective effects of quercetin. Cell viability and mitochondrial function were assessed using CCK-8 assay and Mitotracker staining, while apoptosis, reactive oxygen species (ROS) levels, and myocardial fibrosis were measured. Real-time-quantitative polymerase chain reaction and Western blot analyses were performed to examine the expression of key molecules in the Akt/Bcl-2 pathway, elucidating the molecular mechanisms by which quercetin improves ventricular remodeling and myocardial fibrosis through regulation of this signaling pathway. Results: In H/R-injured H9C2 cells, quercetin significantly enhanced cardiomyocyte survival, inhibited apoptosis, maintained mitochondrial function, and reduced ROS in H/R-injured H9C2 cells. Molecular analysis demonstrated that quercetin regulated the Akt pathway by upregulating Bcl-2 and downregulating P53, thereby reducing apoptosis. In aortic constriction-induced HF rats, quercetin improved cardiac function, attenuated fibrosis, and inhibited ventricular remodeling through activation of the Akt/Bcl-2 signaling pathway. Conclusion: Quercetin mitigates ventricular remodeling and myocardial fibrosis through Akt/Bcl-2 pathway activation, offering a promising therapeutic strategy for CHF.
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