Effects of etomldate postconditlonlng on apoptotds In a rnt model of focal cerebral lschemia-reperhrslon In- jury / 中华麻醉学杂志

ABSTRACT

ObjectiveTo investigate the effects of etomidate postconditioning on apoptosis in a rat model of focal cerebral ischemia-reperfusion(I/R) injury.MethodsThirty-two pathogen-free male SD rats weighing 250-300 g were randomly divided into 4 groups ( n =8 each) using random number tablegroup sham operation ( group S); group focal cerebral I/R; group lipid emulsion (vehicle for etomidate) (group L) and group etomidate postconditioning (group Ep).Focal cerebral I/R was induced by inserting a nylon thread with rounded tip into right internal carotid artery.The thread was advanced cranially until resistance was met.Middle cerebral artery was occluded for 2 h in groups I/R,L and Ep.Normal saline,lipid emulsion and etomidate emulsion 20 mg/kg were injected peritoneally at the end of ischemia in groups I/R,L and Ep respectively.The animals were sacrificed at 24 h of reperfusion and their brains were removed for microscopic examination,assessment of apoptosis (by TUNEL) and detection of Bcl-2 and Bax expression ( by immuno-histochemistry).Apoptosis index ( AI =the number of apoptofic neurons/the total number of neurons examined × 100％ ) and Bcl-2/Bax ratio were calculated.Results I/R induced microscopic changes,significantly increased AI and Bcl-2 Bax ratio and up-regulated Bcl-2 and Bax expression in group I/R as compared with group S.Etomidate postconditioning significantly amefiorated brain damage,decreased AI,increased Bcl-2/Bax ratio,up-regulated Bcl-2 expression and down-regulated Bax expression in ischemic cerebral hemisphere in group Ep as compared with group I/R.There was no significant difference in brain damage,AI and Bcl-2 and Bax expression and Bcl-2/Bax ratio between groups I/R and L.ConclusionEtomidate postconditioning can attenuate focal cerebral ischemia-reperfusion injury in rats by inhibiting apoptosis and modulating Bcl-2 and Bax expression.