Why the study?
Doxorubicin-induced cardiomyopathy is a lethal disease driven by increased redox status and apoptotic signaling, prompting investigation into whether genistein offers cardioprotection.
Key points are not available for this paper at this time.
Population
Mice model
Comparison
Genistein treatment vs doxorubicin-induced cardiotoxicity
Design
Animal experimental study
May support adjunctive testing in doxorubicin recipients; hypothesis-generating and should not change practice.
Doxorubicin (DOX)-induced cardiomyopathy is a lethal disease. DOX-induced cardiotoxic effects are attributed towards increased redox status and apoptotic signaling. In this study, we show that genistein offers protection against DOX-induced cardio toxicity in the mice model. DOX-mediated increase in serum cardiac troponin and redox markers (ROS, LPO, 4-hydroxynonenal-protein adducts [HNE] levels) was significantly reduced by genistein treatment. Significantly increased TNF-α, IL-6, IL-8 expressions during DOX-induced inflammatory responses were down regulated by genistein treatment. Further, we found that genistein regulated antioxidant response through increased Nrf-2, HO-1, NQO1 protein expressions. In addition, DOX downregulated survival proteins (p-Akt, Bcl-2) with concomitant upregulation in Erk (1/2), Bax and cleaved caspase-3 expressions. The apoptotic activation was significantly downregulated by genistein treatment through suppression of apoptosis. Altogether, these findings show that genistein protects against DOX-induced cardiotoxic effects through activation of Nrf-2/HO-1 signaling.
No takes yet. Share an insight, caveat, or question.
Zhifeng et al. (2019) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: