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Genistein protects against doxorubicin‐induced cardiotoxicity through Nrf‐2/HO‐1 signaling in mice model
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.
Genistein protects against doxorubicin‐induced cardiotoxicity through Nrf‐2/HO‐1 signaling in mice model
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.
Genistein protects against doxorubicin‐induced cardiotoxicity through Nrf‐2/HO‐1 signaling in mice model
Bai, Zhifeng (author) / Wang, Zhijian (author)
Environmental Toxicology ; 34 ; 645-651
2019-05-01
7 pages
Article (Journal)
Electronic Resource
English
Nrf‐2 , caspase , inflammation , doxorubicin , genistein
Mitochondrial Amount Determines Doxorubicin‐Induced Cardiotoxicity in Cardiomyocytes
| Wiley | 2025