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 inflammatory and oxidative/nitrosative stress markers in the brain and to investigate the modulation of these markers by minocycline, dexamethasone and vitamin E to establish the best way of its prevention. 60 male albino rats were divided into 5 groups:-control group, hepatic encephalopathy group, hepatic encephalopathy + minocycline group, hepatic encephalopathy + dexamethasone group and hepatic encephalopathy + vitamin E group. Galactosamine injection resulted in significant increase in serum ALT, AST and ammonia and increase in i-NOS gene expression, heme oxygenase-1 gene expression, levels of nitrite/nitrate, IL-1beta, IL-6 and TNF alpha in the brain and significant increase in brain water but resulted in significant decrease in level of IL-10 in the brain 24 hours after injection and death of all animals 48 hours after injection. Minocycline or dexamethasone 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 inflammation and increase oxidative stress in brain after 24 hours and animal death after 48 hours. Minocycline, dexamethasone and vitamin E protected liver and brain from galactosamine induced injury 24 hours after injection but didn't prevent animal death 48 hours after injection.