Selenium protects against bile duct ligation-induced brain damage in male rats: effect on brain ammonia, glutamine and fos gene expression

Abstract

Hepatic encephalopathy (HE) is a severe medical illness often associatedwith liver cirrhosis and characterized by personality changes, intellectual impairment, and decreased consciousness. The exact pathophysiology of HE is debated, but it generally involves neurotoxins, decreased neurotransmission, systemic inflammation, and altered brain energy utilization. The goal of this study is to find out the protective effect of selenium (Se) supplements on the brains of rats with chronic extrahepatic cholestasis caused by bile duct ligation. Thirty albino rats were divided into three groups. Group I: Sham-operated control; group II: bile duct-ligated rats (BDL); and group III: bile duct-ligated rats protected with selenium (BDL-Se), receiving 100 µg/kg/day of selenium orally for six weeks. Following the experimental period, histological and biochemical analyses of liver and brain tissues were performed after sacrifice. Results elucidated that selenium refuced oxidative stress in the brain, indicated by a reduced level of brain malondialdehyde (MDA), an increased level of brain reduced glutathione (GSH), decreased collagen deposition, as well as the intensity of inflammatory infiltrate in liver tissue, the absence of ruptured blood vessels, and degenerated neurons in brain tissue. Additionally, selenium exhibited an anti-inflammatory role by lowering the brain levels of interleukin-1β (IL-1β) and the c-fos gene.