Possible Contribution of Brain Oxidative Stress in Experimental Acute Hepatic Encephalopathy in Rats Role of Minocycline and Vitamin E

Encephalopathy and brain edema are serious complications of liver failure and may lead to rapid death of patients. The present study was designed to show the effects of acute hepatic encephalopathy on the oxidative/nitrosative stress markers in the brain and to investigate the modulation of these markers by minocycline and vitamin E to establish the best way of its prevention. 24 male albino rats were divided into 4 groups: Control group, hepatic encephalopathy group, hepatic encephalopathy+minocycline treated group and hepatic encephalopathy+vitamin E treated group. Galactosamine injection resulted in significant increase in serum ammonia and increase in iNOS gene expression, heme oxygenase-1 gene expression, levels of nitrite/nitrate in the brain and significant increase in brain water. Minocycline or vitamin E injection resulted in partial reversal of measured parameters compared to hepatic encephalopathy group. It can be concluded that galactosamine injection led to hepatic encephalopathy, brain oedema and increase oxidative stress in brain after 24 hours. Minocycline and vitamin E protected liver and brain from galactosamine induced injury 24 hours after injection.