Ascorbic acid attenuates cadmium-induced myocardial hypertrophy and cardiomyocyte injury through Nrf2 signaling pathways comparable to resveratrol.
Ascorbic acid
Cadmium
Myocardial hypertrophy
Nrf2
ROS
Resveratrol
Journal
3 Biotech
ISSN: 2190-572X
Titre abrégé: 3 Biotech
Pays: Germany
ID NLM: 101565857
Informations de publication
Date de publication:
Mar 2023
Mar 2023
Historique:
received:
14
10
2022
accepted:
17
02
2023
pmc-release:
01
03
2024
entrez:
6
3
2023
pubmed:
7
3
2023
medline:
7
3
2023
Statut:
ppublish
Résumé
Chronic cadmium (Cd) exposure severely affects the structural integrity of the heart, leading to cardiovascular disease. This study investigates the protective role of ascorbic acid (AA) and resveratrol (Res) in cellular defense against Cd-induced cardiomyocyte damage and myocardial hypertrophy in H9c2 cardiomyocytes. Experimental results showed that AA and Res treatment significantly increased cell viability, reduced ROS production, attenuated lipid peroxidation, and increased antioxidant enzyme activity in Cd-induced H9c2 cells. AA and Res decreased the mitochondrial membrane permeability and protected the cells from Cd induced cardiomyocyte damage. This also suppressed the pathological hypertrophic response triggered by Cd, which increased the cell size of cardiomyocytes. Gene expression studies revealed that cells treated with AA and Res decreased the expression of hypertrophic genes ANP (two-fold), BNP (one-fold) and β- MHC (two-fold) compared to Cd exposed cells. AA and Res promoted the nuclear translocation of Nrf2 and increased the expression of antioxidant genes (HO-1, NQO1, SOD and CAT) during Cd mediated myocardial hypertrophy. This study proves that AA and Res play a significant role in improving Nrf2 signaling, thereby reversing stress-induced injury, and facilitating the regression of myocardial hypertrophy.
Identifiants
pubmed: 36875963
doi: 10.1007/s13205-023-03527-w
pii: 3527
pmc: PMC9978049
doi:
Types de publication
Journal Article
Langues
eng
Pagination
108Informations de copyright
© King Abdulaziz City for Science and Technology 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
Déclaration de conflit d'intérêts
Conflict of interestThe authors have no competing interests to declare that are relevant to the content of this article.
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