Key result
Astaxanthin treatment increased the resistance of H9c2 cardiomyocytes to H2O2 and doxorubicin-induced cytotoxicity, maintained mitochondrial potential, and reduced reactive oxygen species.
Why the study?
Cardiovascular diseases remain challenging in clinical practice, and astaxanthin is known to penetrate cell membranes, localize in mitochondria, and prevent mitochondrial dysfunction.
Does astaxanthin reduce cell death in H9c2 cardiomyocytes exposed to H2O2 and doxorubicin?
Does astaxanthin reduce cell death in H9c2 cardiomyocytes exposed to H2O2 and doxorubicin?
Astaxanthin protects H9c2 cardiomyocytes against H2O2- and doxorubicin-induced cytotoxicity by preserving mitochondrial function and enhancing mitophagy.
Answers are grounded in this paper and cite their sources.
May protect stressed cardiomyocytes in vitro; leaves open clinical translation pending in vivo studies.
Cardiovascular diseases are among the most challenging problems in clinical practice. Astaxanthin (AST) is a keto-carotenoid (xanthophyll) mainly of marine origin, which is able to penetrate the cell membrane, localize in mitochondria, and prevent mitochondrial dysfunction. In this study effect of astaxanthin on the death of H9c2 cardiomyocytes caused by the cytotoxic effect of hydrogen peroxide (H2O2) and doxorubicin (DOX) was examined. Using methods of spectrophotometry, spectrofluorimetry, and Western blotting analysis, it was shown that treatment of the cells with AST contributed to the increase in the number of H9c2 cells resistant to H2O2 and doxorubicin, while maintaining the value of their mitochondrial transmembrane potential, reducing intracellular production of reactive oxygen species, and increasing intracellular content of the mitophagy markers PINK1, Parkin, and prohibitin 2. The obtained results suggest that the use of AST could be a highly effective way to prevent and treat cardiovascular diseases.
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Krestinin et al. (2024) studied H2O2- and doxorubicin-induced cardiotoxicity. Astaxanthin was evaluated on Cell death, mitochondrial transmembrane potential, reactive oxygen species production, and mitophagy markers. Astaxanthin treatment increased the resistance of H9c2 cardiomyocytes to H2O2 and doxorubicin-induced cytotoxicity, maintained mitochondrial potential, and reduced reactive oxygen species.
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