Antioxidative Effects of Umbelliprenin Against Acrylamide-Induced Hepatotoxicity in Mice

سال انتشار: 1405
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 20

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شناسه ملی سند علمی:

JR_SKUMS-28-2_007

تاریخ نمایه سازی: 17 مهر 1405

چکیده مقاله:

Introduction: Acrylamide (ACR) is a well-known hepatotoxicant commonly found in heat-processed carbohydrate-rich foods, which induces oxidative stress (OS) and liver injury in animal models. Umbelliprenin, a prenyloxy coumarin with documented antioxidant and anti-inflammatory properties, has been proposed as a potential hepatoprotective agent. This experimental study investigated the protective effects of umbelliprenin against ACR-induced hepatotoxicity in adult male albino mice. Methods: Animals were randomly allocated to experimental groups. Mice were divided into control, ACR (۵۰ mg/kg/day, oral), umbelliprenin (۱۲.۵ mg/kg/day, i.p.), ACR + umbelliprenin, and paraffin vehicle groups (n = ۷ per). After ۱۰ days of treatment, serum liver function enzymes (alanine aminotransferase [ALT], aspartate transferase [AST], alkaline phosphatase [ALP], and bilirubin) and OS markers, including malondialdehyde (MDA), total antioxidant capacity (TAC), and glutathione peroxidase (GPx) activity, underwent evaluation. Data were analyzed using SPSS version ۲۶.۰. Results: ACR significantly increased ALT (P = ۰.۰۱۲), AST (P = ۰.۰۰۸), ALP (P = ۰.۰۰۳), bilirubin (P = ۰.۰۴۱), and MDA (P = ۰.۰۱۸) while decreasing TAC (P = ۰.۰۲۷) and GPx activity (P = ۰.۰۲۱), indicating hepatic oxidative damage. Based on the results, umbelliprenin co-administration mitigated these alterations, restoring ALT (vs. ACR group, P = ۰.۰۳۵) and bilirubin (P = ۰.۰۴۸) to near control levels, reducing MDA (P = ۰.۰۳۹), and partially improving TAC (P = ۰.۰۴۴) and GPx activities (P = ۰.۰۴۲). Conclusion: Umbelliprenin exerts hepatoprotective effects against ACR-induced liver injury by enhancing antioxidant defenses, decreasing lipid peroxidation, and preserving liver function, emphasizing its potential as a natural therapeutic factor for chemically induced hepatotoxicity.