Effects of sevoflurane postconditioning on heme oxygenase-1 expression in hippocampal against cerebral ischemia-reperfusion injury

Objective To investigate the effect of sevoflurane postconditioning on heme oxygenase-1(HO-1) expression against cerebral ischemia-reperfusion injury.Methods Forty male SD rats of clean grade weighing 230-270 g were randomly divided into 5 groups: sham operation group (group C), cerebral IR group (group IR), sevoflurane postconditioning group (group S), sevo+Znpp (group SZ) and vehicle group(group SD). An cerebral IR model was established by drawing blood from right carotid vein and immediate 20 min occlusion of bilateral carotid artery.Rats in group S were intubated at 5 minutes before reperfusion, and inhaled 1 MAC sevoflurane for 15 minutes. Rats in group SZ received intraperitoneal injection of Znpp 45 μmol/kg in 0.5 ml DMSO before model established. Rats in group SD received the same volume vehicle and sevoflurane postconditioning. After 24-hour reperfusion, all rats were euthanized and the hippocampus were obtained for pathological observation by light-microscopy and determination of SOD activity, MDA and HO-1 content..Results Compared with group C, SOD activities decreased and MDA contents increased significantly in other four groups (P0.05). There was no significant difference in HO-1 expression between groups C and SZ, while HO-1 expression significantly increased in the other three groups (P0.05). Compared with group IR, SOD activity and HO-1 expression significantly increased and MDA content significantly decreased in groups S and SD (P0.05). There was no significant difference in SOD and MDA between group IR and SZ, while HO-1 was significantly lower in group SZ than that in group IR (P0.05). There was no significant difference in SOD, MDA and HO-1 content between group S and SD. The pathological damage of hippocampal in groups S and SD was greatly relieved in groups S and SD.Conclusion Sevoflurane postconditioning has a protective effect on rat hippocampal against cerebral ischemia-reperfusion, which might be associated with up-regulation of cerebral HO-1 expresion.