Dexamethasone treatment reverses cognitive impairment but increases brain oxidative stress in rats submitted to pneumococcal meningitis

Abstract

Pneumococcal meningitis is associated with a significant mortality rate and neurologic sequelae. The animals received either 10L of saline or a S. pneumoniae suspension and were randomized into different groups: sham: placebo with dexamethasone 0.7mg/kg/1day; placebo with dexamethasone 0.2mg/kg/7days; meningitis groups: dexamethasone 0.7mg/kg/1day and dexamethasone 0.2mg/kg/7days. Ten days after induction we evaluated memory and oxidative stress parameters in hippocampus and cortex. In the step-down inhibitory avoidance task, we observed memory impairment in the meningitis group with dexamethasone 0.2mg/kg/7days. The lipid peroxidation was increased in hippocampus in the meningitis groups with dexamethasone and in cortex only in the meningitis group with dexamethasone 0.2mg/kg/7days. The protein carbonyl was increased in hippocampus in the meningitis groups with dexamethasone and in cortex in the meningitis groups with and without dexamethasone. There was a decrease in the proteins integrity in hippocampus in all groups receiving treatment with dexamethasone and in cortex in all groups with dexamethasone (0.7mg/kg/1day). The mitochondrial superoxide was increased in the hippocampus and cortex in the meningitis group with dexamethasone 0.2mg/kg/7days. Our findings demonstrate that dexamethasone reverted cognitive impairment but increased brain oxidative stress in hippocampus and cortex in Wistar rats ten days after pneumococcal meningitis induction. Copyright © 2011 Tatiana Barichello et al.