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Updated: Mar 28, 2026
A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
Resveratrol protects cardiomyocytes from doxorubicin-induced apoptosis through the AMPK/P53 pathway
Mi-Hua Liu1, Xiao-Long Lin2, Dong-Ming Guo3
1Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
Abstract:
Doxorubicin (DOX) is an efficient drug used in cancer therapy; however, it has severe cardiotoxic side effects. The aim of the present study was to investigate the effects of resveratrol on the adenosine monophosphate-activated protein kinase (AMPK)/P53 pathway in mediating DOX-induced cytotoxicity. H9c2 cells were exposed to 5 µM DOX for 24 h to establish a model of DOX-induced cardiotoxicity. DOX administration amplified P53 and B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) expression and decreased Bcl-2 expression in H9c2 cells. Resveratrol increased the cell viability and decreased the apoptotic rate. In addition, resveratrol markedly increased the phosphorylation of AMPK. Of note, resveratrol protected against DOX-induced increases of P53 and Bax and also prevented the downregulation of Bcl-2 in H9c2 cells. Furthermore, AMPK inhibitor Compound C abolished the protective effects of resveratrol. The results of the present study therefore indicated that resveratrol protected H9c2 cells from DOX-induced apoptosis via the AMPK/P53 pathway.
Insights
Resveratrol protects heart cells from Doxorubicin (DOX) damage by activating the adenosine monophosphate-activated protein kinase (AMPK)/P53 pathway. This natural compound reduces DOX-induced cell death and apoptosis, offering a potential therapeutic strategy.
Area of Science:
- Cardiology
- Pharmacology
- Molecular Biology
Background:
- Doxorubicin (DOX) is a potent chemotherapy agent with significant cardiotoxicity.
- Understanding the molecular mechanisms of DOX-induced cardiotoxicity is crucial for developing protective strategies.
Purpose of the Study:
- To investigate the cardioprotective effects of resveratrol against Doxorubicin (DOX)-induced cardiotoxicity.
- To elucidate the role of the adenosine monophosphate-activated protein kinase (AMPK)/P53 pathway in mediating these effects.
Main Methods:
- H9c2 cells were treated with DOX to model cardiotoxicity.
- The effects of resveratrol on cell viability, apoptosis, and protein expression (P53, Bax, Bcl-2, p-AMPK) were assessed.
- AMPK inhibition using Compound C was employed to confirm pathway involvement.
Main Results:
- DOX treatment increased P53 and Bax expression while decreasing Bcl-2 expression, inducing apoptosis.
- Resveratrol enhanced cell viability, reduced apoptosis, and increased AMPK phosphorylation.
- Resveratrol counteracted DOX-induced changes in P53, Bax, and Bcl-2 levels.
- AMPK inhibition abolished the protective effects of resveratrol.
Conclusions:
- Resveratrol exhibits significant cardioprotective effects against DOX-induced cardiotoxicity.
- These protective effects are mediated through the activation of the AMPK/P53 signaling pathway.
- Resveratrol represents a potential therapeutic agent for mitigating chemotherapy-induced heart damage.
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