Protective efficacy of luteolin against aflatoxinB1-induced toxicity, oxidative damage, and apoptosis in the rat liver.

Abstract

One particularly harmful mycotoxin, aflatoxin B1 (AFB1), usually triggers liver toxicity and oxidative stress in both humans and other mammals. Luteolin (LUTN), a popular active phytochemical molecule, exhibits a strong antioxidant potential. The purpose of this investigation was to explore the potential molecular mechanism in rats and determine if LUTN exhibits protective benefits against AFB1-induced hepatotoxicity. Random selection was used to determine the four treatment groups, each consisting of 24 rats (n = 6). Physiological saline was administered to group 1 (CONT); group 2 received LUTN for a dosage of 50-mg/kg BW. AFB1 was administered to group 3 for a dosage of 0.75-mg/kg BW, and AFB1 with LUTN was given to group 4 at the same dosages mentioned in the previous groups. Rats intoxicated with AFB1 alterations of hepatic transaminases, aspartate aminotransferase (AST) and alanine aminotransferase (ALT), displayed periportal mononuclear cell infiltrations, disorganized lobular architecture, and dispersed necrotic cells in their liver tissues. By reducing serum biochemical levels of the hepatic transaminases ALT and AST brought on by AFB1 exposure, our results demonstrated that LUTN treatment considerably restored liver injury. Through lowering the production of malondialdehyde (MDA) and reactive oxygen species (ROS), as well as by boosting the activity of the antioxidant enzyme catalase (CAT) and superoxide dismutase (SOD), LUTN mitigated the oxidative stress brought on by AFB1. Our findings showed that LUTN significantly reversed the liver damage caused by AFB1. When considered as a whole, LUTN may protect the liver from damage brought on by AFB1 by acting as a potential mitigator and may aid in the creation of cutting-edge therapies to treat liver illnesses in humans and/or animals.