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Acta Biomedica Scientia

Volume 13, Issue 1, 2026
Mcmed International
Acta Biomedica Scientia
Issn
2348 - 215X (Print), 2348 - 2168 (Online)
Frequency
bi-annual
Email
editorabs@mcmed.us
Journal Home page
http://mcmed.us/journal/abs
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Abstract
Title
ROLE OF QUERCETIN IN REDUCING DOXORUBICIN-INDUCED CARDIOMYOCYTE APOPTOSIS AND RESTORING CELLULAR INTEGRITY
Author
Riya Zullah MS, Audinarayana Nelavala
Email
keyword
Quercetin, Doxorubicin, Cardiomyocyte Apoptosis, Cellular Integrity, Proteomic Analysis
Abstract
Cancer has always remained the leading cause of mortality as well as morbidity around the world and thus great efforts have been expended in formulating cancer treatment protocols. The doxorubicin is an effective and widely used to treat cancer, but it also induces reactive oxygen species (ROS) which increases profound toxic effects by causing destruction of cells in the heart. Quercetin is a flavonoid found in plants and it has been acclaimed to possess strong antioxidant and antiinflammatory properties. This in vitro experiment was carried out to explore the assumption that the quercetin may mitigate the cytotoxic effects of doxorubicin and aid in the processes of cell repair in H9C2 cardiomyocytes. The cellular responses to the treat-ment of quercetin in terms of the response of the cell against the quercetin were determined using the proteomic analysis and the cell biology electro-phoresis assays. The results revealed that quercetin had protective effect in cardiomyocyte exposed to a heart damage model of doxorubicin induced heart injury. At least quercetin significantly increased cell survival by affecting its apoptosis and preserving cell morphology via reorganization of the cytoskeleton. Additionally, 2D-DIGE and MALDI-TOF MS analysis indicated that quercetin could enhance cardiomyocyte repair under the influence of metabolic regulation, protein folding plus the re-organization of cytoskeletons post-doxorubicin exposure. This is the first extensive reporting on the protective effect of quercetin against cardiomyocyte toxicity induced by doxorubicin using extensive cellular biology and proteomics studies
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