Key result
Allicin mitigates stanozolol-induced cardiotoxicity, reducing troponin levels by ~60% in a preclinical model.
Why the study?
Anabolic steroids such as stanozolol are popular for muscle-building but dangerous to the heart, prompting evaluation of whether allicin can obstruct stanozolol-induced cardiac injury.
Does allicin prevent stanozolol-induced cardiotoxicity, oxidative stress, and myocardial damage in a rabbit model?
Does allicin prevent stanozolol-induced cardiotoxicity, oxidative stress, and myocardial damage in a rabbit model?
In a rabbit model, allicin significantly mitigated anabolic steroid-induced cardiotoxicity by reducing oxidative stress, inflammation, and myocardial fibrosis, suggesting potential as a cardioprotective agent.
Allicin shows promise against steroid cardiotoxicity in rabbits; hypothesis-generating, leaves human translation open pending trials.
BACKGROUND: There 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. METHODS: Thirty 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. RESULTS: Stanozolol 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. CONCLUSION: Allicin 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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Asker et al. (2025) studied Stanozolol-induced cardiotoxicity (n=30). Allicin vs. Stanozolol alone (0.5 mg/kg body weight) was evaluated on Troponin levels (ng/mL) (p=0.005). Allicin co-administration significantly mitigated stanozolol-induced cardiotoxicity in rabbits, reducing troponin levels from 0.5 ng/mL to 0.2 ng/mL (p=0.005) and improving oxidative and inflammatory markers.
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