Journal of food science and technology(Iran)

Journal of food science and technology(Iran)

Assessment of Cyclophosphamide-Induced Nephrotoxicity in a Preclinical Model and Evaluation of the Protective Efficacy of Sylvestroside I via Modulation of Pro-Inflammatory Cytokine Pathways

Document Type : Original Article

Authors
1 Department of Pharmaceutics, Faculty of Pharmacy, Kufa University, Al-Najaf, Iraq
2 Alkafeel university
3 Jabir Ibn Hayyan University of Medical and Pharmaceutical Sciences
4 Al-Zahrawi University college
5 The Islamic University, Najaf, Iraq.
Abstract
This study investigated the protective efficacy of Sylvestroside I (SYL), a secoiridoid glycoside of potential botanical origin, against CYP-induced renal injury in a preclinical model. Forty male Wistar rats were allocated into four groups: Control, CYP-only (200 mg/kg, i.p.), SYL-only (50 mg/kg/day, oral), and CYP+SYL. After a 30-day experimental period, renal function was assessed via serum creatinine and blood urea nitrogen (BUN). Oxidative stress was evaluated by measuring malondialdehyde (MDA) and total antioxidant capacity (TAC). Pro-inflammatory (TNF-α, IL-6) and protective (IL-22) cytokines were quantified, and renal histopathology was examined. CYP administration significantly impaired renal function, elevated oxidative stress (increased MDA, decreased TAC), disrupted cytokine balance (elevated TNF-α and IL-6, reduced IL-22), and caused severe histopathological damage. Sylvestroside I co-treatment markedly attenuated these effects, normalizing renal biomarkers, enhancing antioxidant status, restoring cytokine levels, and preserving renal tissue architecture. The results demonstrate that Sylvestroside I exerts potent renoprotective effects against CYP-induced toxicity, primarily through antioxidant and anti-inflammatory mechanisms. These findings position Sylvestroside I as a promising candidate for further development within the context of functional ingredients or nutraceutical strategies aimed at supporting renal health and reducing chemical-induced tissue injury.
Keywords

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