ArticleAnimal models and experimental medicine2025
Protective effects of allicin against stanozolol-induced cardiotoxicity: Physiological and histopathological evidence in a rabbit model.
Article in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Physiological, molecular, and histological evaluation of the effects of cobalamin on cardiac function in castrated rabbits.Open veterinary journal · 2026Article
- Protective effects of allicin against stanozolol-induced cardiotoxicity: Physiological and histopathological evidence in a rabbit model.Animal models and experimental medicine · 2025Article
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4 authors.
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Abstract
backgroundThere are many forms of anabolic steroids, including stanozolol (Winstrol), which are popular for their muscle-building effects but dangerous to the heart. This present work is aimed at evaluating the pharmacologica impact of allicin, a natural attribute obtained from garlic, on obstructing cardiac injury in rabbits that received stanozolol.
methodsThirty rabbits were divided into three groups: control, stanozolol-treated, and stanozolol plus allicin. Cardiac function was assessed by measuring troponin, creatine kinase (CK), Galectin-3, and GDF-15. Oxidative stress and antioxidant markers, including malondialdehyde (MDA), glutathione, and catalase, were analyzed. Inflammatory mediators such as C-reactive protein (CRP), interleukin-6 (IL-6), NF-κB, iNOS, nitric oxide (NO), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β) were evaluated. Lipid profile parameters, including total cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL), were measured. Histopathological examination assessed myocardial damage, fibrosis, and collagen deposition.
resultsStanozolol administration significantly increased cardiac damage markers, oxidative stress, and inflammatory mediators while causing dyslipidemia, characterized by elevated LDL and total cholesterol and reduced HDL. Allicin co-administration effectively countered these effects by reducing oxidative stress and inflammation, restoring antioxidant balance, and improving lipid profiles. Histopathological analysis revealed severe myocardial disorganization, necrosis, and fibrosis in the stanozolol group, whereas the allicin-treated group exhibited preserved myocardial structure with reduced collagen deposition.
conclusionAllicin significantly mitigates stanozolol-induced cardiotoxicity by reducing oxidative stress, inflammation, lipid dysregulation, and myocardial damage, as evidenced by biochemical and histopathological findings. These results suggest that allicin may serve as a potential therapeutic agent to counteract the cardiovascular risks associated with anabolic steroid use.
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