摘要
目的研究颅脑损伤(TBI)后钠通道α亚单位1.3(Nav1.3)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,在伤后2h、12h、24h和72h处死,取伤侧海马行荧光定量PCR和Western blot检测Nav1.3的mRNA和蛋白表达情况,通过免疫荧光染色检测Nav1.3在海马的表达特点。结果大鼠脑液压伤后Nav1.3的mRNA表达显著上调(P<0.01),伤后12h其上调达最高水平,而Nav1.3蛋白的表达也在相同时间段出现显著上调(P<0.01)。免疫荧光染色显示Nav1.3在海马主要表达于神经元细胞。结论TBI可导致Nav1.3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 investigate the expression of Nav1.3 mRNA and protein in the hippocampus following traumatic brain injury (TBI). Methods The lateral fluid percussion model was established in adult male Sprague Dawley rats. The mRNA and protein levels of Nav1.3 in ipsilateral hippocampus at 2, 12, 24 and 72 h post-TBI were measured using RT-PCR and Western blot techniques. Immunofluorescenee analyses were performed to detect the cellular distribution of Nav1.3 in the hippocampus. Results The mRNA of Nav1.3 was significantly up-regulated (P〈0.01) following TBI and reached the peak at 12 h post-TBI. The protein of Nav1.3 was up-regulated too at the same time (P〈0.01). The result of immunofluorescence analyses showed that the Nav l.3 expressed mainly in neurons in the hippocampus. Conclusion TBI could cause significant up-regulation of Nav1.3 mRNA and protein, which may be related to the molecular mechanism of functional alternation of sodium channels and excitotoxic conditions following TBI.
出处
《中国微侵袭神经外科杂志》
CAS
北大核心
2009年第2期77-80,共4页
Chinese Journal of Minimally Invasive Neurosurgery
基金
国家重点基础研究项目(编号:2005CB522604)
国家自然科学基金(编号:30571908)
上海市领军人才和上海市医学领军人才基金
关键词
颅脑损伤
钠通道
神经保护
craniocerebral traumatic
sodium channels
neruo-protection