Objective To investigate the effects of dexmedetomidine 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 Sprague-Dawley rats, aged 6 weeks, weighing 200~250g, were randomly divided into 3 groups (n=8 each): control group(group C), LPS group(group E)and dexmedetomidine group(group D). Dexmedetomidine 50 ug/kg was injected intrapefitoneally and LPS 5mg/kg was injected via caudal vein 30 min later in group D. Normals 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 12h, the cognitive function of rats were tested by Morris maze, the rats were sacrificed and hippocampal were harvest at each group. Terminal-deoxynucleotidyl transfer 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 the number of crossing the platform was decreased in group  E[（55±17）s, （905±126）cm, (4.8±1.4)times] and D[(37±13)s, (534±114)cm, （9.5±3.9）times]（P<0.05）; Bcl-2 immunopositivity remains at constantly level in group E(P>0.05), while Bax[11.2±1.7] immunopositivity was increased, the Bcl-2/Bax ratio [0.73±0.12]was decreased(P<0.05); The expression of Bcl-2[12.2±2.9] and Bax[9.1±2.1] were upregulated in group D, Bcl-2/Bax ratio [1.53±0.24]was increased(P<0.05). Compared with group E, the AI index [2.72±2.54]was decreased, Bcl-2 expression was upregulated while Bax expression was downregulated, Bcl-2/Bax ratio was increased in group D(P<0.05). Conclusion dexmedetomidine can improve the cognitive function of rats with endotoxemia, and its mechanism may be related to the regulation of Bcl-2 and Bax, decreasing the neuronal apoptosis in hippocampus.