右美托咪啶对创伤性脑损伤大鼠海马区神经元自噬的影响  

Effect of dexmedetomidine on hippocampal neuronal autophagy of rats with traumatic brain injury

作　　者：谷志杰[1] 张满和[2] 周秀敏[2] 邢彦杰[2] 赵昕[2] 张树立[2] 

机构地区：[1]河北省唐山市乐亭县医院,河北乐亭063600 [2]河北省唐山工人医院,河北唐山063000

出　　处：《实用临床医药杂志》2016年第9期14-16,共3页Journal of Clinical Medicine in Practice

摘　　要：目的探讨右美托咪啶对创伤性脑损伤(TBI)大鼠海马区神经元自噬的影响。方法采用改良自由落体装置制备成年SD大鼠脑损伤模型,TBI后立即静脉注射右美托咪啶15μg/kg。采用神经损伤评分评价运动功能,Morris水迷宫测试大鼠空间学习能力。LC3和Neu N的共定位。免疫印迹分析LC3的表达量。结果与TBI组比较,Dex组NSS差值显著降低(P<0.05)。与sham组比较,TBI后所有大鼠在24、48 h逃避潜伏期显著增加(P<0.05)。与TBI组比较,Dex组在48 h逃避潜伏期显著缩短(P<0.05)。与TBI组比较,Dex组显着抑制6、12、24 h的LC3Ⅱ上调(P<0.05)。结论 TBI后应用右美托咪啶能显著改善运动和认知功能,抑制海马区神经元的细胞自噬,促进神经功能的恢复。Objective To explore the effect of dexmedetomidine（ Dex） on hippocampal neuronal autophagy of rats with traumatic brain injury（ TBI）. Methods The modified free fall device was used to prepare models of adult SD rats with TBI,and 15 μg / kg Dex was administered immediately after TBI. Motor function was assessed by Neurologic Severity Score（ NSS）,and the spatial learning ability was evaluated by Morris water maze. The co-localization of microtubule-associated protein 1 light chain 3（ LC3） and neuronal nuclei（ Neu N） was made. Expression of LC3 was detected by Western blot analysis. Results Compared with TBI group,the NSS score decreased significantly in Dex group（ P〈 0. 05）. Compared with sham group,escape latency at 24,48 h in all rats after TBI increased significantly（ P〈 0. 05）. Compared with TBI group,escape latency at 48 h significantly decreased in Dex group（ P〈 0. 05）. Compared with TBI group,the up-regulations of LC3 at 6,12 and 24 h were significantly inhibited in Dex group（ P〈 0. 05）. Conclusion Application of Dex after TBI can significantly improve motor and cognitive functions,inhibit hippocampal neuronal autophagy and promote the recovery of neural function.

关 键 词：创伤性脑损伤 右美托咪啶 水迷宫 自噬 海马区 神经功能 

分 类 号：R651.1[医药卫生—外科学]