Effect Of Sevoflurane Postcondionting On Neuronal Apoptosis After Cerebral Ischemia-reperfusion Injury In Rats

Objective To investigate effect of sevoflurane postconditioning on neuronal apoptosis aftercerebral ischemia-reperfusion injury in rats and the role of PI3K/Akt signaling pathway inwhich.Methods Forty male SD rats which were from Shanxi medical university animal experimentcenter with250-270g body-weight were randomly divided into five groups(with8rats each): Cgroup,ischemia-reperfusion(IR group),2.5%sevoflurane postconditioning group(S group),2.5%sevoflurane+LY294002group (S+LY group) and DMSO group． The global cerebralischemia/reperfusion(I/R)was induced by bilateral common cephalic artery occlusion andmaintained20min combined with hypotension. We observed the morphological changes ofhippocampal neurons by HE. To examine the apoptotic pyramidal neuron by TUNEL test and theexpression of caspase-3and p-Akt were observed by immunohistochemical method.Results1) The result of light microscopy: In C group,neuron cells were normal. Cytoplasmwas rich. The nuclei were round.Compared with C group, IR group showed severe injury. Theneuron cells were lighter in S group than IR group.2) The result of the myocardium apoptosisindex: Compared with C group, AI in IR group and S groups were significantlyhigher(P<0.05).Compared with IR group, AI in S groups were significantly lower(P<0.05).3)The result of myocardium Caspase-3and p-Akt protein:Compared with C group, thecaspase-3expression and p-Akt expression were significantly increased in other four group(P<0.05).Compared with IR group, the caspase-3expression were significantly decreased, p-Aktexpression was significantly increased in S group(P<0.05).There was no sianificant difference inall variables among IR group、S+LY group and DMSO group(P>0.05).Conclusion1） Apoptosis neurons exists in cerebral ischemia and reperfusion processsevoflurane postcondionting can reduce apoptosis neurons.2）Sevoflurane postcondnioning canprotect brain IR injury in rat by decreased the expression of caspase-3and this antiapoptoticeffect may be achieved by activation of PI3K/Akt signaling pathway.