The Protective Effect Of Dexmedetomidine On The Brain Against Incomplete Ischemia Reperfusion Injury In The Rats

ObjectiveTo investigate the protective effect and mechanism ofdexmedetomidine on thebrain against incomplete ischemia reperfusion injury in the rats.MethodsSixty four male SD rats weighing200-300g were randomly divided into4equal groups: ctrl group(Ctrl), ischemia reperfusion model group(Mod),ischemia-reperfusion group treated by5ug·kg-1·h-1dexmedetomidine(Dex2), ischemia-reperfusion group treated by Pdtc200mg/kg before the operation(Pdtc). The middle cerebral arteryocclusion(MCAO) models were established with the method ofintraluminal suture occlusion. After ischemia reperfusion for24h, theneurologic deficit score(NDS) was evaluated. The area of cerebralinfarction was observed by the TTC stain. The levels of seruminflammatory cytokines TNF-α, IL-6and the apoptotic index of thehippocampal region、the expression of NF-kb in striatum、hippocampaland cerebral cortex region was separately detected by Elisa array、TUNELstaining、Western Blot. ResultsThere were no neurologic deficits in rats of the Ctrl group、Mod group、Dex2group and Pdtc group, while there were significant cerebralinfarction in rats of the Mod group and Dex2group、Pdtc group. Comparedto Mod group, the cerebral infarction area were significantly decreased inDex2group and Pdtc group.Compared to the Ctrl group, the levels of serum inflammatorycytokines TNF-α, IL-6was significantly increased in Mod group、Dex2group and Pdtc group. But, the levels of serum inflammatory cytokinesTNF-α, IL-6was also significantly decreased in Dex2group and in Pdtcgroup than in Mod group (p<0.05).The apoptotic index of Dex2group and Pdtc group was significantlyless than that of Mod group(p<0.05). Compared to the Ctrl group, thepositive expression of NF-κB in striatum、hippocampal and cerebral cortexregion was significantly increased in Mod group、Dex2group and Pdtcgroup. In the hippocampal and cerebral cortex, the positive expression ofNF-κB was significantly lower in Dex2group and in Pdtc group than inMod group (p<0.05); but in cerebral striatum, the positive expression ofNF-κB showed no difference in Mod group、Dex2group and Pdtc group.ConclusionsDex5ug·kg-1·h-1can reduce the area of the cerebral infarction andsuppress apoptosis of hippocampal CA1region in rats with incompletecerebral ischemia reperfusion． Dexmedetomidine could inhibit the expression of NF-κB in hippocampal and cerebral cortex region．Thismay be the mechanism of dexmedetomidine in cerebral protection．...