Effect of dexmedetomidine on neuronal apoptosis during cerebral ischemia-reperfusion injury
Objective To study the effect of dexmedetomidine on neuronal apoptosis induced by cerebral ischemia-reperfusion injury.Methods Totally,45 male SD rats were randomly divided into sham surgery group(Sham group),model group(MCAO group),and dexmedetomidine group(MCAO+D group)by using a random number table method.In the Sham group,only blood vessels were dissected and separated without blocking blood flow.After embolization of the right middle cerebral artery for 2 h in the MCAO group,blood flow was opened for 24 h.The rats in the MCAO+D group were immediately in-traperitoneally injected with 50 μg/kg dexmedetomidine after reperfusion.The neurological deficits score was evaluated by Longa method,the volume of cerebral infarction was measured by triphenyltetrazolium chloride(TTC)staining,and the pathological changes of cortical neurons in ischemic area were observed by hematoxylin and eosin(HE)staining,the expressions of nod-like receptor pyrin domain containing pro-tein 3(NLRP3),cysteinyl aspartate-specific protease(Caspase)-1 and interleukin(IL)-1β were detected in cerebral cortex by Western blotting,and the ultrastructural changes of neurons were observed by trans-mission electron microscopy.The results were analyzed by analysis of variance and Student's t test.Results Compared with the Sham group,both the MCAO group and the MCAO+D group showed an in-crease in neurological deficit scores after 2 h of ischemia[(2.47±0.64)and(2.40±0.51)points vs.0 point,F=133.300,P＜0.05].In MCAO group,significant infarcted brain tissue areas was observed[(29.41±3.78)％vs.0％,t=-17.388,P＜0.05];the cortical neurons were disordered and irregular,and had nuclear pyknosis and fragmentation;the expression of NLRP3,Caspase-1,and IL-1 β increased in the cerebral cortex tissue(1.28±0.05 vs.0.46±0.09,1.35±0.12 vs.0.41±0.15,1.30±0.09 vs.0.53±0.07,t=-13.103,-8.538,-12.115,all P＜0.05).Compared with the MCAO group,the MCAO+D group showed a significant decrease in neurological deficit score[(2.60±0.63)points vs.(1.33±0.49)points,t=0.148,P＜0.05],decreased infarct volume in brain tissue[(14.09±2.50)％vs.(29.41±3.78)％,t=-7.552,P＜0.05],improved neuronal morphology,and decreased expression of NLRP3,Caspase-1 and IL-1 β in cortical tissue after 24 h of reperfusion(0.79±0.08 vs.1.28±0.06,0.76±0.09vs.1.35±0.11,0.91±0.13 vs.1.30±0.09,t=-8.903,-7.077,-4.407,all P＜0.05).Conclusion Dexmedetomidine can improve neurological dysfunction caused by cerebral ischemia-reperfusion injury,reduce infarct volume of brain tissue,alleviate neuronal necrosis,and has a protective effect on cerebral ischemia-reperfusion injury in rats.
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