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Updated: Dec 1, 2025

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
[Prevention of Diastolic Dysfunction Caused by Doxorubicin by Mitochondrial Antioxidant Plastomitin]
V L Lakomkin1, A A Abramov1, E V Lukoshkova1
1National Medical Research Center of Cardiology, Ministry of Healthcare Russian Federation, Moscow.
Abstract:
Aim An attempt to prevent the development of diastolic dysfunction (DD) with the mitochondrial antioxidant plastomitin on a model of doxorubicin-induced cardiomyopathy. DD is a type of chronic heart failure. Due to the increasing number of patients with this condition and the absence of effective therapy, development of means for DD correction is a relevant objective.Material and methods Cardiomyopathy was modeled in 17 rats by two subcutaneous injections of doxorubicin 2 mg/kg/week. The other group (n=17), also administered with doxorubicin, received plastomicin 0.32 mg/kg daily subcutaneously. Left ventricular function was evaluated with echocardiography (EchoCG) and cardiac catheterization with simultaneous pressure and volume monitoring.Results According to EchoCG data the ejection fraction remained unchanged in the experimental groups. Cardiac catheterization showed disorders of both myocardial contractility and relaxability only in the doxorubicin group.Conclusion A course of plastomitin in combination with the doxorubicin treatment can maintain normal heart contractility and thereby, prevent the known doxorubicin cardiotoxicity.
Insights
Plastomitin, a mitochondrial antioxidant, prevented doxorubicin-induced heart problems in rats. This study suggests plastomitin can protect heart contractility during doxorubicin treatment, preventing cardiotoxicity.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Diastolic dysfunction (DD) is a form of chronic heart failure with increasing prevalence and limited therapeutic options.
- Doxorubicin is a common chemotherapy agent known to cause cardiotoxicity, leading to heart failure.
- Mitochondrial dysfunction plays a key role in the development of doxorubicin-induced cardiotoxicity and diastolic dysfunction.
Purpose of the Study:
- To investigate the potential of plastitomin, a mitochondrial antioxidant, in preventing doxorubicin-induced diastolic dysfunction (DD) and cardiotoxicity.
- To evaluate the protective effects of plastitomin on left ventricular function in a rat model of doxorubicin-induced cardiomyopathy.
Main Methods:
- Cardiomyopathy was induced in rats using doxorubicin injections.
- One group received doxorubicin with plastitomin, while the control group received doxorubicin alone.
- Left ventricular function was assessed using echocardiography (EchoCG) and cardiac catheterization.
Main Results:
- Echocardiography revealed no significant changes in ejection fraction between the groups.
- Cardiac catheterization demonstrated impaired myocardial contractility and relaxability exclusively in the doxorubicin-only group.
- Plastomitin administration concurrently with doxorubicin preserved normal heart contractility.
Conclusions:
- A course of plastitomin combined with doxorubicin treatment effectively prevented doxorubicin-induced cardiotoxicity.
- Plastomitin shows promise in maintaining normal cardiac function during doxorubicin chemotherapy.
- This study highlights the potential of mitochondrial antioxidants in managing chemotherapy-related heart damage.
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