Protective Role of Vanillic Acid Against Sodium Arsenite-Induced Cardiotoxicity in Male Mice: A Focus on Antioxidant and Anti-inflammatory Properties
| Author | Mohammad Javad Khodayar | en |
| Author | Maryam Shirani | en |
| Author | Shokooh Mohtadi | en |
| Author | Mohammad Amin Behmanesh | en |
| Author | Reza Azadnasab | en |
| Author | Saeedeh Shariati | en |
| Orcid | Mohammad Javad Khodayar [0000-0001-9518-1286] | en |
| Orcid | Maryam Shirani [0000-0002-9397-1767] | en |
| Orcid | Mohammad Amin Behmanesh [0000-0002-4292-5381] | en |
| Orcid | Reza Azadnasab [0000-0002-3438-9419] | en |
| Orcid | Saeedeh Shariati [0000-0002-6771-8901] | en |
| Issued Date | 2025-11-30 | en |
| Abstract | Background: Cardiovascular diseases (CVDs) remain a leading cause of mortality worldwide, and their growing prevalence has been associated with exposure to environmental toxicants such as sodium arsenite (SA). Objectives: The present study aimed to evaluate the potential cardioprotective effects of vanillic acid (VA) against SA-induced cardiotoxicity (CTX) in male NMRI mice. Methods: In an 8-week experimental study, 30 male NMRI mice were randomly assigned to five groups (n = 6 per group). The control group received saline. One group received drinking water containing SA (50 ppm), another was treated with VA (100 mg/kg), and two groups received combined treatments of SA (50 ppm) plus VA at doses of 50 mg/kg or 100 mg/kg. The VA was administered orally during the final two weeks of the study. At the end of the treatment period, serum biomarkers, oxidative stress (OS) parameters, and inflammatory cytokines were measured. Results: The SA exposure significantly increased serum levels of creatine kinase-MB (CK-MB), aspartate transaminase (AST), and lactate dehydrogenase (LDH), as well as OS markers and inflammatory indices. Treatment with VA markedly lowered these cardiac injury biomarkers and improved OS parameters, including superoxide dismutase (SOD) and catalase (CAT) activities. The VA administration also enhanced peroxisome proliferator-activated receptor gamma (PPARγ) expression and reduced nuclear factor kappa B (NF-κB) levels, indicating possible mechanisms underlying its protective role. Conclusions: The findings suggest that VA exerts cardioprotective effects against SA-induced cardiac injury, likely through modulation of OS and inflammatory signaling pathways, supporting its potential as a therapeutic agent in SA-related CTX. | en |
| DOI | https://doi.org/10.5812/jjnpp-166500 | en |
| Keyword | Vanilic Acid | en |
| Keyword | Soudium Arsenite | en |
| Keyword | Cardiotoxicity | en |
| Keyword | Mice | en |
| Publisher | Brieflands | en |
| Title | Protective Role of Vanillic Acid Against Sodium Arsenite-Induced Cardiotoxicity in Male Mice: A Focus on Antioxidant and Anti-inflammatory Properties | en |
| Type | Research Article | en |