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Quercetin attenuates doxorubicin cardiotoxicity by modulating Bmi-1 expression
Qinghua Dong1, Long Chen, Qunwei Lu
1Central Lab of Biomedical Research Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
British Journal of Pharmacology
|June 7, 2014
Summary
Quercetin protects against doxorubicin-induced cardiotoxicity by up-regulating Bmi-1 expression, reducing oxidative stress and apoptosis. This offers a potential strategy for preventing chemotherapy-related heart damage.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Doxorubicin chemotherapy can cause cardiotoxicity, limiting its use.
- Quercetin has shown protective effects against doxorubicin-induced liver damage previously.
Purpose of the Study:
- To investigate quercetin's protective effects against doxorubicin-induced cardiotoxicity.
- To explore the role of Bmi-1 (a regulator of mitochondrial function and ROS generation) in quercetin's protective mechanism.
Main Methods:
- Evaluated quercetin's effects on doxorubicin-induced cardiotoxicity in H9c2 cardiomyocytes and C57BL/6 mice.
- Assessed apoptosis, mitochondrial function, oxidative stress, and related signaling pathways.
- Measured cardiac function, serum enzyme activity, and reactive oxygen species (ROS) in mice.
Main Results:
- Quercetin reduced doxorubicin-induced apoptosis, mitochondrial dysfunction, ROS, and DNA damage in H9c2 cells.
- Quercetin increased Bcl-2 and Bmi-1 expression while decreasing Bid, p53, and oxidase expression.
- In mice, quercetin mitigated cardiac dysfunction, reduced ROS and lipid peroxidation, and enhanced Bmi-1 and superoxide dismutase expression.
Conclusions:
- Quercetin mitigates doxorubicin-induced cardiotoxicity in vitro and in vivo.
- This protection is mediated by reduced oxidative stress through the upregulation of Bmi-1 expression.
- Findings suggest quercetin as a potential therapeutic agent for preventing doxorubicin-induced cardiomyopathy.

