Hepatic encephalopathy (HE) is a prevalent complication of the central nervous system (CNS) that is caused by acute or chronic liver failure. This study was designed to evaluate the effects of thymoquinone (TQ) on thioacetamide (TAA)-induced HE in rats, and determine the consequential behavioral, biochemical, and histological changes. HE was induced in male Wistar rats by intraperitoneal (i.p.) injection of 200 mg/kg TAA once every 48 h for 14 consecutive days. Control groups received the normal saline containing 5 % DMSO. Thymoquinone (5, 10, and 20 mg/kg) was administered for ten consecutive days intraperitoneally (i.p.) after HE induction and it was continued until the end of the tests. Then, the passive avoidance memory, extracellular single unit, BBB permeability, and brain water content were evaluated. Moreover, hippocampal tissues were used for evaluation of oxidative stress index, inflammatory biomarkers, and histological parameters following HE. As result of the treatment, TQ improved passive avoidance memory, increased the average number of simultaneous firing of spikes/bins, improved the integrity of BBB, and decreased brain water content in the animal model of HE. Furthermore, the results indicated that treatment with TQ decreased the levels of inflammatory cytokines (TNF-α and IL-1β) but increased the levels of glutathione (GSH) and anti-inflammatory cytokine (IL-10) of the surviving cells in the hippocampal tissues. This study demonstrates that TQ may have beneficial therapeutic effects on cognitive, oxidative stress, neuroinflammatory, and histological complications of HE in rat.
Keywords: Cognition; Extracellular single unite; Hepatic encephalopathy; Inflammatory markers; Thymoquinone.