{"title":"黄芪单体槲皮素在调节Akt/Bcl-2通路改善慢性心力衰竭心室重构中的作用及机制","authors":"Sailing Hu, Lingchun Lv, Wuming Hu","doi":"10.4103/ijabmr.ijabmr_97_25","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>Quercetin mitigates ventricular remodeling and myocardial fibrosis through Akt/Bcl-2 pathway activation, offering a promising therapeutic strategy for CHF.</p>","PeriodicalId":13727,"journal":{"name":"International Journal of Applied and Basic Medical Research","volume":"15 3","pages":"184-196"},"PeriodicalIF":0.8000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12422554/pdf/","citationCount":"0","resultStr":"{\"title\":\"Role and Mechanism of Astragalus Monomer Quercetin in Modulating Akt/Bcl-2 Pathway to Improve Ventricular Remodeling in Chronic Heart Failure.\",\"authors\":\"Sailing Hu, Lingchun Lv, Wuming Hu\",\"doi\":\"10.4103/ijabmr.ijabmr_97_25\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>Quercetin mitigates ventricular remodeling and myocardial fibrosis through Akt/Bcl-2 pathway activation, offering a promising therapeutic strategy for CHF.</p>\",\"PeriodicalId\":13727,\"journal\":{\"name\":\"International Journal of Applied and Basic Medical Research\",\"volume\":\"15 3\",\"pages\":\"184-196\"},\"PeriodicalIF\":0.8000,\"publicationDate\":\"2025-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12422554/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Applied and Basic Medical Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4103/ijabmr.ijabmr_97_25\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/8/20 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Applied and Basic Medical Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/ijabmr.ijabmr_97_25","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/8/20 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
Role and Mechanism of Astragalus Monomer Quercetin in Modulating Akt/Bcl-2 Pathway to Improve Ventricular Remodeling in Chronic Heart Failure.
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.