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右美托咪定对创伤性脑损伤大鼠认知功能和P2 X7表达的影响
引用本文:郑彬,张顺才,曾彦茹,李平,付晓东,阮祥才,许立新,佘守章.右美托咪定对创伤性脑损伤大鼠认知功能和P2 X7表达的影响[J].广东医学,2016(12):1761-1763.
作者姓名:郑彬  张顺才  曾彦茹  李平  付晓东  阮祥才  许立新  佘守章
作者单位:1. 广州医科大学附属广州市第一人民医院麻醉科 510180;2. 广州医科大学基础医学院生理学教研室 广州510180
基金项目:广东省医学科研基金资助项目(编号A2013502)
摘    要:目的:观察右美托咪定( Dex )对创伤性脑损伤( TBI )大鼠认知功能和海马炎性反应的影响,探讨P2X7在其中的作用机制。方法雄性3~4月龄SD大鼠80只随机分为4组( n=20)。建立TBI模型,Dex组和TBI+Dex组连续4 d腹腔注射盐酸Dex注射液20μg/kg,对照组和TBI组连续4 d腹腔注射生理盐水;TBI后第7天各组均行Moris水迷宫实验观察大鼠认知功能变化,酶联免疫吸附( ELISA )法检测大鼠海马组织中白细胞介素-1β(IL-1β)浓度,Western blot检测海马组织中P2X7的表达。结果与对照组比较,TBI组行为学训练第3~5天逃避潜伏期明显延长,探索时间明显缩短(P<0.05);与TBI组比较,TBI+Dex组训练第3~5天逃避潜伏期缩短,探索时间延长(P<0.05);TBI组海马IL-1β含量明显高于其他3组(P<0.001);与对照组比较,TBI组P2X7表达明显上调(P<0.001);与TBI组比较,TBI+Dex组P2X7表达明显降低(P<0.001)。与对照组比较, Dex组训练第3~5天逃避潜伏期、探索时间、海马IL-1β含量和P2X7表达差异均无统计学意义(P>0.05)。结论 Dex可改善TBI引起的认知功能障碍,其作用机制可能是Dex抑制P2X7活性,进而降低海马区域炎性反应,改善认知功能。

关 键 词:创伤性脑损伤  神经炎症  认知功能障碍  右美托咪定  P2X7

Effects of dexmedetomidine on cognitive function and hippocampus P2X7 expression in rats with traumatic brain injury
Abstract:Objective To observe the effects of Dexmedetomidine ( Dex) on cognitive function and neuroinflam-mation after traumatic brain injury (TBI), and to discuss the possible mechanism of P2X7 receptor in these effects. Methods Eighty Male SD rats (3~4 months old) were randomly divided into control group , Dex group, TBI group, and TBI+Dex group (n=20).The TBI model was established.Intraperitoneal Dex (20μg· kg-1) was given to the subjects in Dex group and TBI+Dex group , while saline was given in control group and TBI group .Moris water maze test was per-formed to evaluate the cognitive function 6 days after TBI .ELISA was used to quantify the concentration of interleukin -1β(IL-1β) in hippocampus.Western blot was used to measure the expression of P 2X7 in hippocampus.Results Compared with control group , the escape latency was significantly prolonged , with the time of staying at the original plat-form quadrant shortened, between Day 3 and 5 in TBI group (P<0.05);meanwhile, the concentration of IL -1β, and the expression of P2X7 in hippocampus were significantly increased in TBI group ( P <0.001).Compared with TBI group, the escape latency was significantly shortened , with the time of staying at the original platform quadrant prolonged in TBI+Dex group (P<0.05); meanwhile, the concentration of IL -1β, and the expression of P2X7 in hippocampus were significantly reduced in TBI +Dex group (P<0.001).Conclusion Dexmedetomidine can attenuate TBI -induced cognitive decline and neuroinflammation via inhibiting the activity of P 2X7 receptor.
Keywords:traumatic brain injury  neuroinflammation  cognitive dysfunction  dexmedetomidine  P2X7
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