Effect of dexmedetomidine pretreatment on hippocampus Bcl-2, Bax expression and cognitive function in endotoxemia rat

Abstract

Objective To investigate the effects of dexmedetomidine(Dex) pretreatment on endotoxemia rats cognitive function and the expression of Bcl-2 and Bax in hippocampus. Methods A total of twenty-four pathogen-free male SD rats, aged 6 weeks, weighing 200-250 g, were randomly divided into 3 groups(n=8): control group(group C), lipopolysaccharide(LPS) group(group E) and Dex group(group D). Dex 50 μg/kg was injected intraperitoneally and LPS 5 mg/kg was injected via caudal vein 30 min later in group D. Normal saline 2 ml was injected intraperitoneally and LPS 5 mg/kg was injected via the caudal vein in 30 min later in group E. Normal saline 2 ml was injected intraperitoneally and then injected via the caudal vein 30 min later in group C. After administration of 12 h, the cognitive function of rats were tested by Morris maze, the rats were sacrificed and hippocampal were harvest at each group. Terminal-deoxynucleotidyl transfering mediated nick end labeling was applied to evaluate the apoptosis index(AI). The expression of protein Bcl-2 and Bax were detected by immunohistochemical method. Results Compared with group C, the latency and swimming distance were increased and numbers of crossing the platform were decreased in group E and D(P 0.05) while Bax immunopositivity was increased. The Bcl-2/Bax ratio was decreased(P<0.05), the expression of Bcl-2 and Bax were upregulated in group D, Bcl-2/Bax ratio was increased(P<0.05). Compared with group E, the AI index was decreased, Bcl-2 expression was upregulated while Bax expression was downregulated, Bcl-2/Bax ratio was increased in group D(P<0.05). Conclusions Dex can improve the cognitive function of rats with endotoxemia. Its mechanism is related to the regulating expression level of Bcl-2 and Bax with a result of decreasing the neuronal apoptosis in hippocampus. Key words: Dexmedetomidine; Endotoxemia; Bcl-2; Bax