Coriander seed oil extract abrogates hepatic biochemical and histopathological alterations associated with acrylamide intoxication in rats

Abstract

Acrylamide (ACR) is a byproduct of the Maillard reaction and is known to cause oxidative insults. Coriandrum sativum seed oil (CSO) exhibits documented antioxidant, anti-inflammatory, and anti-apoptotic, making it a potential protective agent against toxicant-induced tissue damage. This study was designed to assess the anti-inflammatory, antioxidant, and anti-apoptotic characteristics of CSO versus ACR-induced hepatotoxicity in rats. Rats were placed into four equal groups: the control, the ACR group (25 mg/kg), the CSO group (600 mg/kg), and the CSO + ACR. All groups were treated for 21 days. The current findings showed that body weight significantly ( P <0.05) decreased by 66%, and blood liver enzymes increased following ACR treatment. Malondialdehyde and nitric oxide levels were elevated significantly in the liver tissue in response to ACR, while superoxide dismutase, catalase activity, and glutathione levels were decreased. Inflammatory response in terms of nuclear factor-κB, tumour necrosis factor-alpha, interleukin-1beta and interleukin 12 in liver tissue were significantly ( P <0.05) raised. Moreover, the pro-apoptotic markers Bax and caspase-3 were significantly elevated after ACR intoxication, while, Bcl-2 levels were decreased. Interestingly, hepatotoxicity, oxidative stress, inflammation, and apoptosis brought on by ACR toxicity were lessened markedly with CSO treatment. Overall, this study's findings point to the significance of CSO in restricting the hepatotoxicity induced by ACR, mainly due to its antioxidative constituents. • Acrylamide (ACR) induces hepatotoxicity. • Coriandrum sativum seed oil (CSO) exhibits significant hepatoprotective effectiveness against ACR-mediated liver toxicity • CSO suppresses various mechanisms, such as oxidative stress, the NF-κB pathway, and apoptosis.