右美托咪定对脑缺血再灌注损伤大鼠大脑皮质Wnt/β-catenin蛋白表达的影响

Effect of dexmedetomidine on Wnt/β-catenin protein expression in cerebral cortex of rats with cerebral ischemia-reperfusion injury

目的观察右美托咪定对脑缺血再灌注损伤大鼠大脑皮质Wnt/β-catenin蛋白表达的影响。方法将48只雄性SD大鼠按随机区组的原则分为三组:对照组、模型组和右美托咪定组,每组各16只。采用大脑中动脉阻塞(Middle cerebral artery occlusion,MCAO)法制造大鼠脑缺血再灌注损伤模型。右美托咪定组于缺血1 h即刻经尾静脉注射1μg/kg右美托咪定作为负荷剂量,持续10 min,随后以0.5μg/(kg·h)的速率静脉输注至脑缺血2 h。对照组和模型组大鼠按相同方法给予生理盐水。再灌注24 h时进行神经功能评分后处死大鼠取出脑组织,各组取8只大鼠脑组织行TTC染色法测定脑梗死体积,另8只大鼠采用Western blot法检测大脑皮质β-catenin蛋白表达量。结果与对照组相比,模型组大鼠神经行为学评分明显增加[(3.00±0.82)vs(0±0),P<0.05]、脑梗死体积明显增加[(64.23±6.72)%vs(0±0)%,P<0.05],β-catenin蛋白表达量明显减少(0.46±0.14 vs 1.12±0.23,P<0.05)。与模型组相比,右美托咪定组大鼠神经行为学评分(1.69±0.71 vs 3.00±0.82,P<0.05)、脑梗死体积明显减少[(45.13±8.29)%vs(64.23±6.72)%,P<0.05],β-catenin蛋白表达量明显增加[(0.82±0.23)vs(0.46±0.14),P<0.05]。结论右美托咪定能减轻大鼠脑缺血再灌注损伤,其机制可能与增加大脑皮质中β-catenin蛋白表达量有关。

Objective To observe the effect of dexmedetomidine on Wnt/β-catenin protein expression in cerebral cortex of rats with cerebral ischemia-reperfusion injury.Methods A total of 48 male SD rats were divided into 3 groups according to the principle of randomized block:control group,model group and dexmedetomidine group,with 16 rats in each group.The middle cerebral artery occlusion(MCAO)method was used to make the model of cerebral ischemia-reperfusion injury in rats.In the dexmedetomidine group,1μg/kg dexmedetomidine was injected into caudal vein as a loading dose for 10 min immediately after 1 h of ischemia,and then was injected intravenously to cerebral ischemia for 2 h at a rate of 0.5μg/(kg·h).Rats in the control group and the model group were given normal saline in the same way.Neurological function scores were concluded 24 h after reperfusion,and then rats were executed for brain tissues to be taken out.Brain tissues of 8 rats in each group were taken out for TTC staining method to measure cerebral infarction volume,and the expression ofβ-catenin protein in cerebral cortex of the other 8 rats was detected by Western blot method.Results Compared with the control group,in the model group the neurobehavioral scores of the rats were significantly increased(3.00±0.82 vs 0±0,P<0.05),the cerebral infarction volume was significantly increased[(64.23±6.72)%vs(0±0)%,P<0.05],and the expression ofβ-catenin protein was significantly decreased(0.46±0.14 vs 1.12±0.23,P<0.05).Compared with the model group,in the dexmedetomidine group,the neurobehavioral scores of the rats(1.69±0.71 vs 3.00±0.82,P<0.05)and the cerebral infarction volume[(45.13±8.29)%vs(64.23±6.72)%,P<0.05]were significantly reduced,and the expression ofβ-catenin protein[(0.82±0.23)vs(0.46±0.14),P<0.05]was significantly increased.Conclusion Dexmedetomidine can reduce cerebral ischemia-reperfusion injury in rats,and its mechanism may be related to increasing the expression ofβ-catenin protein in cerebral cortex.