ArticleInternational journal of molecular sciences2025
The Role of the Wnt/β-Catenin Pathway in the Modulation of Doxorubicin-Induced Cytotoxicity in Cardiac H9c2 Cells by Sulforaphane and Quercetin.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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3 authors.
Funding
Abstract
This study investigates the role of sulforaphane (SFN) and quercetin (QCT) in alleviating the oxidative stress and modulation of cellular responses induced by doxorubicin (DOX) in rat cardiomyoblast cells H9c2. The potential mechanisms involving Wnt/β-catenin signaling and antioxidant response were determined. We found that SFN effectively mitigated DOX-induced cytotoxicity in H9c2 cells. These effects of SFN significantly exceeded the influence of QCT. Levels of superoxide dismutase isoforms 1 (SOD-1) and 2 (SOD-2) were upregulated following SFN and QCT pretreatment in cells exposed to effects of DOX. Additionally, β-catenin levels were increased following both SFN and QCT treatment, even in the presence of doxorubicin. Elevated β-catenin levels for QCT were associated with increased phosphorylation and inactivation of glycogen synthase kinase 3-β. The critical role of Wnt/β-catenin signaling in responses of H9c2 cells to effects of DOX was confirmed using Wnt/β-catenin inhibitor WIKI-4. This inhibitor increased the sensitivity of cells to DOX, and the decreased cellular viability after pretreatment with WIKI-4 was linked to SOD activities' inhibition. Conclusively, sulforaphane and quercetin exert a protective effect against doxorubicin-induced cytotoxicity in H9c2 cells through the Wnt/β-catenin pathway as well as in association with modulation of enzymes related to the cellular antioxidant response.
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