Shahrekord University of Medical Sciences Journal of Shahrekord University of Medical Sciences 2717-0071 28 2 2026 07 29 Antioxidative Effects of Umbelliprenin Against Acrylamide-Induced Hepatotoxicity in Mice 98 103 10.34172/jsums.1154 EN Firoozeh Saghaei https://orcid.org/0000-0002-7997-6190 Maryam Karimi-Dehkordi https://orcid.org/0000-0001-6086-2014 Journal Article 10.34172/jsums.1154 2026 05 03 2026 05 25 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 (50 mg/kg/day, oral), umbelliprenin (12.5 mg/kg/day, i.p.), ACR + umbelliprenin, and paraffin vehicle groups (n = 7 per). After 10 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 26.0. Results: ACR significantly increased ALT (P = 0.012), AST (P = 0.008), ALP (P = 0.003), bilirubin (P = 0.041), and MDA (P = 0.018) while decreasing TAC (P = 0.027) and GPx activity (P = 0.021), indicating hepatic oxidative damage. Based on the results, umbelliprenin co-administration mitigated these alterations, restoring ALT (vs. ACR group, P = 0.035) and bilirubin (P = 0.048) to near control levels, reducing MDA (P = 0.039), and partially improving TAC (P = 0.044) and GPx activities (P = 0.042). 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.