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Updated: Mar 19, 2026
A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
Paeoniflorin inhibits doxorubicin-induced cardiomyocyte apoptosis by downregulating microRNA-1 expression
Jian-Zhe Li1, Xiu-Neng Tang1, Ting-Ting Li2
1Department of Pharmacy, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.
Abstract:
Doxorubicin (DOX) is an effective anthracycline anti-tumor antibiotic. Because of its cardiotoxicity, the clinical application of DOX is limited. Paeoniflorin (PEF), a monoterpene glucoside extracted from the dry root of Paeonia, is reported to exert multiple beneficial effects on the cardiovascular system. The present study was designed to explore the protective effect of PEF against DOX-induced cardiomyocyte apoptosis and the underlying mechanism. In cultured H9c2 cells, PEF (100 µmol/l) was added for 2 h prior to exposure to DOX (5 µmol/l) for 24 h. Cell viability, creatine kinase activity, cardiomyocyte apoptosis, intracellular reactive oxygen species (ROS) levels, and the expression of microRNA-1 (miR-1) and B-cell lymphoma 2 (Bcl-2) were measured following treatment with PEF and/or DOX. The results showed that treatment with DOX notably induced cardiomyocyte apoptosis, concomitantly with enhanced ROS generation, upregulated miR-1 expression and downregulated Bcl-2 expression. These effects of DOX were significantly inhibited by pretreatment of the cells with PEF. These results suggest that the inhibitory effect of PEF on DOX-induced cardiomyocyte apoptosis may be associated with downregulation of miR-1 expression via a reduction in ROS generation.
Insights
Paeoniflorin (PEF) protects heart cells from Doxorubicin (DOX) damage by reducing apoptosis and reactive oxygen species (ROS). This study reveals PEF
Area of Science:
- Cardiovascular Pharmacology
- Molecular Cardiology
- Natural Product Chemistry
Background:
- Doxorubicin (DOX) is a vital chemotherapy agent but its clinical use is limited by cardiotoxicity.
- Paeoniflorin (PEF), derived from Paeonia, shows potential cardiovascular benefits.
- Understanding PEF's protective mechanisms against DOX-induced heart damage is crucial.
Purpose of the Study:
- To investigate the protective effects of Paeoniflorin (PEF) against Doxorubicin (DOX)-induced cardiomyocyte apoptosis.
- To elucidate the underlying molecular mechanisms involved in PEF's cardioprotective action.
Main Methods:
- H9c2 cells were treated with PEF before Doxorubicin (DOX) exposure.
- Assessed cell viability, creatine kinase activity, apoptosis, and intracellular reactive oxygen species (ROS).
- Measured expression levels of microRNA-1 (miR-1) and B-cell lymphoma 2 (Bcl-2).
Main Results:
- Doxorubicin (DOX) induced significant cardiomyocyte apoptosis, increased ROS, upregulated miR-1, and downregulated Bcl-2.
- Pretreatment with Paeoniflorin (PEF) markedly inhibited these DOX-induced detrimental effects.
- PEF treatment reversed DOX-induced changes in cell viability and apoptosis markers.
Conclusions:
- Paeoniflorin (PEF) demonstrates significant cardioprotective effects against Doxorubicin (DOX)-induced apoptosis.
- PEF's mechanism may involve the reduction of ROS generation, leading to miR-1 downregulation.
- PEF holds promise as a therapeutic agent to mitigate Doxorubicin cardiotoxicity.
