摘要
目的研究大鼠颅脑创伤后Nav 1．1和Nav 1．2的mRNA和蛋白在海马中的表达情况。方法对成年SD大鼠实施脑液压伤后分别在伤后2，12，24和72h处死，取伤侧海马行荧光定量PCR和Western blot以及免疫荧光染色等方法检测Nav 1．1和Nav 1．2的mRNA和蛋白表达情况。结果大鼠脑液压伤后Nav 1．1和Nav 1．2的mRNA表达显著下调（P〈0．01），伤后2h即下调至最低水平，Nav 1．1的蛋白表达在颅脑创伤后显著下调（P〈0．01），但伤后72h时恢复至接近对照组的水平。而颅脑创伤后Nav 1．2的蛋白表达水平与对照组相比，差异无统计学意义（P〉0．05）。结论颅脑创伤导致了大鼠海马钠通道仅亚单位mRNA和蛋白表达的显著改变，这可能是颅脑创伤后神经元细胞膜上的钠通道功能异常及其诱发的兴奋性毒性作用的分子学基础之一。
Objective To investigate the mRNA and protein expressions of Nav 1. 1 and Nav 1. 2 in hippocampus following traumatic brain injury （TBI） in rats. Methods After the lateral fluid percussion model was established in adult male Sprague Dawley rats, the rats were sacrificed at 2,12,24 and 72 hours after percussion and collected ipsilateral hippocampus for detecting mRNA and protein expressions of Nav 1. 1 and Nav 1. 2 by means of fluorescent quantitation RT-PCR, Western blot and immunofluorescence staining. Results The mRNA expressions of Nav 1.1 and Nay 1.2 were significantly down-regulated （P 〈 0.01 ） in hippocampus and reached the lowest level at 2 hours following TBI. The protein expression of Nav 1. 1 was significantly down-regulated （P 〈 0.01 ） but recovered near to level of control group at 72 hours after TBI. While there was no statistical difference on protein expression of Nav 1.2 in hippocampus after TBI compared with control group （ P 〉 0.05 ）. Conclusion TBI induces significant down-regulated mRNA and protein expressions of Nav 1.1 in the hippocampus, which may be one of molecular mechanisms for functional alternation of sodium channels and exeitotoxic action following TBI.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2009年第4期309-313,共5页
Chinese Journal of Trauma
基金
国家重点基础研究发展规划资助项目（2005CB522604）
国家自然科学基金资助项目（30571908）
上海市领军人才和上海市医学领军人才基金资助项目
关键词
脑损伤
钠通道
海马
神经保护
Brain injuries
Sodium channels
Hippocampus
Neuroprotection
