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J Shahrekord Univ Med Sci. 2026;28(2): 98-103.
doi: 10.34172/jsums.1154
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Original Article

Antioxidative Effects of Umbelliprenin Against Acrylamide-Induced Hepatotoxicity in Mice

Firoozeh Saghaei 1 ORCID logo, Maryam Karimi-Dehkordi 1* ORCID logo

1 Department of Veterinary, Shk.C., Islamic Azad University, Shahrekord, Iran
*Corresponding Author: Email: ma_karimivet58@iau.ac.ir

Abstract

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.


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Submitted: 03 May 2026
Revision: 23 May 2026
Accepted: 25 May 2026
ePublished: 10 Sep 2026
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