Astaxanthin Protects Against H<sub>2</sub>O<sub>2</sub>- and Doxorubicin-Induced Cardiotoxicity in H9c2 Rat Myocardial Cells

Astaxanthin (AST) is a carotenoid that has positive effects on various organs and tissues. It also exhibits a cardioprotective action. In this study, the influence of AST on the survival of H9c2 cardiomyocytes under hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)- and doxorubi...

Full description

Saved in:
Bibliographic Details
Main Authors: Roman Krestinin, Margarita Kobyakova, Yulia Baburina, Linda Sotnikova, Olga Krestinina
Format: Article
Language:English
Published: MDPI AG 2024-11-01
Series:Life
Subjects:
Online Access:https://www.mdpi.com/2075-1729/14/11/1409
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850068381447749632
author Roman Krestinin
Margarita Kobyakova
Yulia Baburina
Linda Sotnikova
Olga Krestinina
author_facet Roman Krestinin
Margarita Kobyakova
Yulia Baburina
Linda Sotnikova
Olga Krestinina
author_sort Roman Krestinin
collection DOAJ
description Astaxanthin (AST) is a carotenoid that has positive effects on various organs and tissues. It also exhibits a cardioprotective action. In this study, the influence of AST on the survival of H9c2 cardiomyocytes under hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)- and doxorubicin (DOX)-induced cardiotoxicity was investigated. Under these conditions, the content of cytosolic Ca<sup>2+</sup> was measured, and changes in the area of the mitochondrial mass, as well as in the content of the voltage-dependent anion channel 1 (VDAC1), the autophagy marker LC3A/B, and the pro-apoptotic transcription factor homologous protein (CHOP), were determined. It was found that AST removed the cytotoxic effect of H<sub>2</sub>O<sub>2</sub> and DOX, while cell survival increased, and the mitochondrial mass did not differ from the control. At the same time, a decrease in the content of cytosolic Ca<sup>2+</sup> and the restoration of the VDAC1 level to values close to the control were observed. The restoration of the CHOP level suggests a reduction in endoplasmic reticulum (ER) stress in cells. The results allow us to consider AST as a potential agent in the prevention and/or treatment of cardiac diseases associated with oxidative stress.
format Article
id doaj-art-43da940cf9224fc6b2c4f236e53965b5
institution DOAJ
issn 2075-1729
language English
publishDate 2024-11-01
publisher MDPI AG
record_format Article
series Life
spelling doaj-art-43da940cf9224fc6b2c4f236e53965b52025-08-20T02:48:05ZengMDPI AGLife2075-17292024-11-011411140910.3390/life14111409Astaxanthin Protects Against H<sub>2</sub>O<sub>2</sub>- and Doxorubicin-Induced Cardiotoxicity in H9c2 Rat Myocardial CellsRoman Krestinin0Margarita Kobyakova1Yulia Baburina2Linda Sotnikova3Olga Krestinina4Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, 142290 Pushchino, RussiaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, 142290 Pushchino, RussiaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, 142290 Pushchino, RussiaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, 142290 Pushchino, RussiaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, 142290 Pushchino, RussiaAstaxanthin (AST) is a carotenoid that has positive effects on various organs and tissues. It also exhibits a cardioprotective action. In this study, the influence of AST on the survival of H9c2 cardiomyocytes under hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)- and doxorubicin (DOX)-induced cardiotoxicity was investigated. Under these conditions, the content of cytosolic Ca<sup>2+</sup> was measured, and changes in the area of the mitochondrial mass, as well as in the content of the voltage-dependent anion channel 1 (VDAC1), the autophagy marker LC3A/B, and the pro-apoptotic transcription factor homologous protein (CHOP), were determined. It was found that AST removed the cytotoxic effect of H<sub>2</sub>O<sub>2</sub> and DOX, while cell survival increased, and the mitochondrial mass did not differ from the control. At the same time, a decrease in the content of cytosolic Ca<sup>2+</sup> and the restoration of the VDAC1 level to values close to the control were observed. The restoration of the CHOP level suggests a reduction in endoplasmic reticulum (ER) stress in cells. The results allow us to consider AST as a potential agent in the prevention and/or treatment of cardiac diseases associated with oxidative stress.https://www.mdpi.com/2075-1729/14/11/1409astaxanthinH9c2 cellscytotoxicitydoxorubicinmitochondriaautophagy
spellingShingle Roman Krestinin
Margarita Kobyakova
Yulia Baburina
Linda Sotnikova
Olga Krestinina
Astaxanthin Protects Against H<sub>2</sub>O<sub>2</sub>- and Doxorubicin-Induced Cardiotoxicity in H9c2 Rat Myocardial Cells
Life
astaxanthin
H9c2 cells
cytotoxicity
doxorubicin
mitochondria
autophagy
title Astaxanthin Protects Against H<sub>2</sub>O<sub>2</sub>- and Doxorubicin-Induced Cardiotoxicity in H9c2 Rat Myocardial Cells
title_full Astaxanthin Protects Against H<sub>2</sub>O<sub>2</sub>- and Doxorubicin-Induced Cardiotoxicity in H9c2 Rat Myocardial Cells
title_fullStr Astaxanthin Protects Against H<sub>2</sub>O<sub>2</sub>- and Doxorubicin-Induced Cardiotoxicity in H9c2 Rat Myocardial Cells
title_full_unstemmed Astaxanthin Protects Against H<sub>2</sub>O<sub>2</sub>- and Doxorubicin-Induced Cardiotoxicity in H9c2 Rat Myocardial Cells
title_short Astaxanthin Protects Against H<sub>2</sub>O<sub>2</sub>- and Doxorubicin-Induced Cardiotoxicity in H9c2 Rat Myocardial Cells
title_sort astaxanthin protects against h sub 2 sub o sub 2 sub and doxorubicin induced cardiotoxicity in h9c2 rat myocardial cells
topic astaxanthin
H9c2 cells
cytotoxicity
doxorubicin
mitochondria
autophagy
url https://www.mdpi.com/2075-1729/14/11/1409
work_keys_str_mv AT romankrestinin astaxanthinprotectsagainsthsub2subosub2subanddoxorubicininducedcardiotoxicityinh9c2ratmyocardialcells
AT margaritakobyakova astaxanthinprotectsagainsthsub2subosub2subanddoxorubicininducedcardiotoxicityinh9c2ratmyocardialcells
AT yuliababurina astaxanthinprotectsagainsthsub2subosub2subanddoxorubicininducedcardiotoxicityinh9c2ratmyocardialcells
AT lindasotnikova astaxanthinprotectsagainsthsub2subosub2subanddoxorubicininducedcardiotoxicityinh9c2ratmyocardialcells
AT olgakrestinina astaxanthinprotectsagainsthsub2subosub2subanddoxorubicininducedcardiotoxicityinh9c2ratmyocardialcells