Abstract
BackgroundCancer has continually been the leading cause of death worldwide for decades. Thus, scientists have actively devoted themselves to studying cancer therapeutics. Doxorubicin is an efficient drug used in cancer therapy, but also produces reactive oxygen species (ROS) that induce severe cytotoxicity against heart cells. Quercetin, a plant-derived flavonoid, has been proven to contain potent antioxidant and anti-inflammatory properties. Thus, this in vitro study investigated whether quercetin can decrease doxorubicin-induced cytotoxicity and promote cell repair systems in cardiomyocyte H9C2 cells.ResultsProteomic analysis and a cell biology assay were performed to investigate the quercetin-induced responses. Our data demonstrated that quercetin treatment protects the cardiomyocytes in a doxorubicin-induced heart damage model. Quercetin significantly facilitated cell survival by inhibiting cell apoptosis and maintaining cell morphology by rearranging the cytoskeleton. Additionally, 2D-DIGE combined with MALDI-TOF MS analysis indicated that quercetin might stimulate cardiomyocytes to repair damage after treating doxorubicin by modulating metabolic activation, protein folding and cytoskeleton rearrangement.ConclusionBased on a review of the literature, this study is the first to report detailed protective mechanisms for the action of quercetin against doxorubicin-induced cardiomyocyte toxicity based on in-depth cell biology and proteomic analysis.
Highlights
Cancer has continually been the leading cause of death worldwide for decades
To investigate the role of quercetin in alleviating doxorubicin-induced cardiotoxicity, we examined the protective ability of quercetin in doxorubicin-treated rat cardiomyocytes by performing cell biological assays, such as cell viability and apoptotic analysis, as well as a quantitative proteomic analysis based on 2D-Differential gel electrophoresis (DIGE) and MALDI-TOF MS identification [18]
Quercetin facilitates cell survival and maintains cell morphology in doxorubicin-induced cell death in H9C2 cells To evaluate the effect of doxorubicin on rat cardiomyocytes (H9C2), we exposed the cells to doxorubicin in a range of 0-1 μM for 24 h in a serum-free medium
Summary
Cancer has continually been the leading cause of death worldwide for decades. scientists have actively devoted themselves to studying cancer therapeutics. Doxorubicin is an efficient drug used in cancer therapy, and produces reactive oxygen species (ROS) that induce severe cytotoxicity against heart cells. A plant-derived flavonoid, has been proven to contain potent antioxidant and anti-inflammatory properties. This in vitro study investigated whether quercetin can decrease doxorubicin-induced cytotoxicity and promote cell repair systems in cardiomyocyte H9C2 cells. The principal mechanism of doxorubicin is chelating DNA, inhibiting topoisomerase II and producing free radicals to kill cancer cells. Because myocardia are sensitive to reactive oxygen species (ROS), cumulative doxorubicin in vivo causes irreversible damage to heart cells, restricting clinical use of this drug [4].
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