Cardioprotection by

Background: Cyclophosphamide (CTX) is a widely used chemotherapeutic agent whose routine administration can induce cardiotoxicity, limiting its therapeutic efficacy. 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