ArticleAvicenna journal of medical biotechnology
Swimming Exercise Attenuates DOX-Induced Cardiotoxicity by Modulating Apoptosis and DRP1/PGC1α/miR-23a Dependent Pathway in Rat Heart Tissue.
Article in Avicenna journal of medical biotechnology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Doxorubicin (DOX) is a widely used drug in cancer chemotherapy, but its cardiotoxicity limits its clinical applications. Combining exercise with chemotherapy offers a promising approach to mitigate the side effects of chemotherapy drugs. Limited information is available on the effects of swimming exercise on the molecular mechanisms related to DOX cardiotoxicity. This study aims to investigate the modulatory effect of swimming exercise on the apoptosis and Methods: In this experimental study, thirty-two adult male Wistar desert rats (200-220 Results: These findings revealed that DOX administration led to a significant decrease in the cardiac expression of PGC-1α and DRP-1 proteins and an increase in apoptotic proteins (caspase 3 and cytochrome C) compared to the control group (p<0.0001). Swimming exercise resulted in a significant increase expression in cardiac tissue of PGC-1α and DRP-1 proteins and a decrease in the expression of apoptotic proteins in the DOX-treated group (p<0.0001, p<0.01). Compared to the control group, the protein levels in the heart of the Conclusion: These findings suggest that swimming exercise may protect against DOX-induced cardiotoxicity by regulating apoptosis and DRP1/PGC1α/miR-23a pathway. This highlights exercise as a potential non-pharmacological strategy to mitigate chemotherapy-related heart damage.
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