Key result
Allium ampeloprasum extract mitigates cyclophosphamide-induced cardiotoxicity in mice by curbing oxidative stress and inflammation.
Why the study?
Cyclophosphamide is a widely used chemotherapeutic agent that can induce cardiotoxicity, and Allium ampeloprasum subsp. Iranicum extract has been proposed as a natural cardioprotective agent.
Hypothesis-generating for Allium ampeloprasum in cyclophosphamide cardiotoxicity; leaves open translation to human patients.
Background Cyclophosphamide (CTX) is a widely used chemotherapeutic agent whose routine administration can induce cardiotoxicity, limiting its therapeutic efficacy. Allium ampeloprasum subsp. Iranicum extract (AAE) has been proposed as a natural cardioprotective agent owing to its rich phenolic and flavonoid content. This study investigates the protective potential and underlying mechanisms of AAE against CTX-induced cardiotoxicity. Methods NMRI mice were assigned to control, CTX, AAE, and AAE+CTX groups. We assessed: (i) body and heart weight metrics; (ii) histopathology of cardiac tissue; (iii) serum cardiac injury markers (AST, LDH, CK-MB); (iv) myocardial lipid peroxidation (TBARS); (v) antioxidant enzyme activities (SOD, CAT, GSH-Px); (vi) proinflammatory cytokines (TNF-α, IL-6, IL-1β); and (vii) histological heart status as a cross-tissue readout. Data were analyzed for significance against the CTX-alone and control groups. Results CTX induced marked cardiotoxicity, evidenced by weight loss, cardiac histopathology disruptions, elevated TBARS, depleted SOD, CAT, and GSH-Px activities, and increased serum AST, LDH, CK-MB, TNF-α, IL-6, and IL-1β. Pretreatment with AAE markedly mitigated CTX effects: TBARS were reduced; SOD, CAT, and GSH-Px activities were restored or enhanced; serum cardiac injury markers declined; and proinflammatory cytokines decreased. Body weight loss associated with CTX was attenuated, with AAE-associated weight gain surpassing controls. Histology showed preservation of myocardial architecture and reduced vacuolization in cardiac tissue. Conclusion Collectively, these findings indicate that AAE exerts multi-targeted protection through antioxidant, anti-inflammatory, and cytoprotective actions, thereby attenuating CTX-induced cardiotoxicity. These findings position the Iranian accession of A. ampeloprasum as a promising nutraceutical adjunct to CTX therapy, with potential to enhance tolerance and preserve cardiac function. Further work should characterize bioactive constituents, assess pharmacokinetics and interactions with CTX, and explore translational applicability in clinical setting.
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Abedi et al. (2026) studied Cyclophosphamide-induced cardiotoxicity. Allium ampeloprasum subsp. Iranicum extract (AAE) vs. Cyclophosphamide (CTX) alone and control was evaluated on Cardiotoxicity, oxidative stress, and inflammatory markers. Pretreatment with Allium ampeloprasum subsp. Iranicum extract mitigated cyclophosphamide-induced cardiotoxicity in mice by reducing oxidative stress and inflammatory mediators.
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