Ellagic Acid Prevents Oxidative Stress, Inflammation, and Histopathological Alterations in Acrylamide-Induced Hepatotoxicity in Wistar Rats.

The present study was designed to investigate the changes in rat liver tissue after administration of acrylamide (ACR) and ellagic acid (EA). The latter compound was applied for its strong antioxidant and anti-inflammatory properties. In the present study, 35 male Wistar rats were randomly divided into five equal groups. These groups were normal saline (NS), ACR (20 mg/kg), ACR + EA (10 and 30 mg/kg EA), and EA (30 mg/kg). At the end of the experiment, the rats were decapitated. Biochemical and histopathological studies were conducted on liver and serum samples. ACR administration significantly decreased hepatic GSH level, SOD, GPx, and CAT activity when compared to the NS group. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), nitric oxide (NO), protein carbonyl (PC), malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β) levels increased as a result of ACR administration. Administration of EA (more potently at a dose of 30 mg/kg) resulted in a significant reversal of biochemical, inflammatory, and hepatic markers in ACR-intoxicated rats. These biochemical and inflammatory disturbances were supported by histopathological observations of the liver. Our results indicate that EA might be useful for the treatment of the hepatotoxicity induced by ACR via ameliorative effects on biochemical, oxidative stress, and inflammatory indices.