〔Abstract〕 Objective To investigate the effects of dexmedetomidine on inflammatory factors and endoplasmic reticulum stress in myocardial ischemia reperfusion induced brain injury. Methods Twenty-four SPF-grade healthy male SD rats, weighing(200～220)g and aged(6～8) weeks, were divided into three groups(n=8) by random number table method: sham operation group(S group), myocardial ischemia reperfusion group(IR group) and myocardial ischemia/reperfusion+Dex group(IR+Dex group). After the rats were adapted to the feeding environment, the myocardial ischemia reperfusion injury model was established by ligating the anterior descending branch of the left coronary artery for 30 min and reperfusion for 120 min. At the beginning of reperfusion, IR+Dex group was given 25 μg/kg dexmedetomidine, S group and IR group were injected with equal volume normal saline. Rats were sacrificed by decapitation and brain tissue was taken and the changes of hippocampal cell structure of rats stained by HE were observed under light microscope. Serum inflammatory factors IL-6, IL-8 and IL-10 were detected by ELISA. The expressions of Chop, Bip, p-eif-2α and p-perk in rat hippocampal tissues were determined by Western blot. Results Compared with the S group, the IR group and the IR+Dex group showed aggravation of brain lesions, increased expression of inflammatory cytokines IL-6 and IL-8(P<0.05), and decreased expression of IL-10(P<0.05). Hippocampal Chop, Bip, p-eif-2α and p-perk proteins were up-regulated(P<0.05). Compared with IR group, IR+Dex group showed reduced pathological injury, decreased expression of IL-6 and IL-8(P<0.05), increased expression of IL-10(P<0.05), and down-regulated expressions of Chop, Bip, p-eif-2α and p-perk in hippocampal tissues(P<0.05). Conclusion Dexmedetomidine preconditioning can reduce the brain injury caused by myocardial ischemia reperfusion, and its mechanism may be related to the inhibition of systemic inflammatory response and endoplasmic reticulum stress.