ArticleAntioxidants (Basel, Switzerland)2025
Sinapic Acid Ameliorates Doxorubicin-Induced Cardiotoxicity in H9c2 Cardiomyoblasts by Inhibiting Oxidative Stress Through Activation of the Nrf2 Signaling Pathway.
Article in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Self-Assembled Berberine-Sinapic Acid Nanomedicine for Synergistic Chemotherapy.Molecules (Basel, Switzerland) · 2026Article
- From brain to body: sinapic acid prevents multi-organ damage post-traumatic brain injury in mice.Metabolic brain disease · 2026Article
- Doxorubicin Toxicity and Recent Approaches to Alleviating Its Adverse Effects with Focus on Oxidative Stress.Molecules (Basel, Switzerland) · 2025Review
- Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025Review
- Phenolic acids in fermented foods: microbial biotransformation, antioxidant mechanisms, and functional health implications.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The use of doxorubicin (Dox) is restricted because of its cardiotoxicity, which poses a significant mortality risk for cancer patients, despite being a highly effective antibiotic for treating various types of cancer. Therefore, identifying substances or developing preventive strategies against Dox-induced cardiotoxicity is crucial. This study was conducted to determine whether sinapic acid (SA), a phenolic compound with a range of pharmacological effects, could protect against Dox-induced cardiotoxicity in H9c2 cardiomyoblasts. To investigate the preventive effect of SA, H9c2 cardiomyoblasts treated with Dox were pretreated with SA at various concentrations. SA effectively rescued the cells from Dox-induced cardiotoxicity. Additionally, SA significantly reduced oxidative stress by inhibiting mitochondrial dysfunction and endoplasmic reticulum stress. SA also suppressed the expression of MAPK proteins. As for the underlying mechanism of SA's protective effect against Dox-induced cardiotoxicity, SA activated nuclear factor erythroid-2-related factor (Nrf2) by facilitating its movement from the cytosol to the nucleus and increasing the expression of its target antioxidative genes. In summary, this study demonstrated that SA protects H9c2 cardiomyoblasts from Dox-induced cardiotoxicity by inhibiting oxidative stress by the activation of Nrf2-related signaling pathway. Our findings enhance the development of therapeutic strategies to mitigate cardiac toxicity caused by Dox, highlighting the potential antioxidant effect of SA in Dox-treated H9c2 cardiomyoblasts.
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