Astaxanthin Reduces H₂O₂- and Doxorubicin-Induced Cardiotoxicity in H9c2 Cardiomyocyte Cells

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Roman R. Krestinin¹, Margarita I. Kobyakova¹, Yuliya L. Baburina¹, Linda D. Sotnikova¹, Olga V. Krestinina^1,a*

¹Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, 142290 Pushchino, Moscow Region, Russia

^* To whom correspondence should be addressed.

Received: June 18, 2024; Revised: September 17, 2024; Accepted: September 18, 2024

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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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KEY WORDS: astaxanthin, cardiomyocytes, cytotoxicity, mitochondrial dysfunction, mitophagy

DOI: 10.1134/S0006297924100122

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