大鼠颅脑创伤后Na_V1.6在海马的表达  

Expression of Na_V1.6 in hippocampus after traumatic brain injury in rats

作　　者：毛青[1] 贾锋[1] 张晓华[1] 邱永明[1] 葛建伟[1] 吴日乐[1] 张兴福 罗其中[1] 江基尧[1] 

机构地区：[1]上海交通大学医学院仁济医院神经外科,上海200127 [2]安徽省寿县红十字会医院神经外科,寿县232251

出　　处：《上海交通大学学报（医学版）》2009年第4期399-403,共5页Journal of Shanghai Jiao tong University:Medical Science

基　　金：国家重点基础研究发展规划项目(“九七三”计划)(2005CB522604);国家自然科学基金(30571908);上海市医学领军人才培养计划~~

摘　　要：目的研究颅脑创伤(TBI)后NaV1.6的mRNA和蛋白在海马中的表达变化。方法对成年SD大鼠实施脑液压伤,分别在伤后2、12、24和72 h处死大鼠,取伤侧海马行Real-time PCR和Western blotting,检测NaV1.6的mRNA和蛋白表达。结果大鼠脑液压伤后2 h,NaV1.6 mRNA表达显著上调(P<0.001),伤后12 h达最高水平;NaV1.6蛋白表达显著上调,并持续至伤后72 h(P<0.01)。结论TBI可导致NaV1.6的mRNA和蛋白表达显著上调,这可能是TBI后神经元细胞膜上钠通道功能异常及其诱发兴奋性毒性作用的分子学基础之一。Objective To detect the expression of Navl. 6 mRNA and protein in hippocampus after traumatic brain injury （TBI）. Methods The lateral fluid percussion models were established with adult SD rats. The expression of Nav1. 6 mRNA and protein in ipsilateral hippoeampus 2, 12, 24 and 72 h after TBI were detected by Real-time PCR and Western blotting, respectively. Results The expression of Nav0. 6 mRNA was significantly up-regulated 2 h after TBI （P 〈 0. 001） , and reached the peak 12 h after TBI. The expression of Nav1. 6 protein was significantly up-regulated after TBI and maintained until 72 h after TBI （P 〈 0.01 ）. Conclusion TBI causes significant up-regulation of expression of Nav1. 6 mRNA and protein, which may be related to the molecular mechanism of functional alternation of sodium channels and excitotoxic conditions following TBI.

关 键 词：颅脑创伤 液压伤 钠通道 Nav1.6 神经保护 

分 类 号：R651.15[医药卫生—外科学]