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细胞黏附分子(ICAM-1)在大鼠弥漫性脑损伤中的表达意义
引用本文:王翀,朱贤立,赵洪洋,李玉,李金星,赵甲山.细胞黏附分子(ICAM-1)在大鼠弥漫性脑损伤中的表达意义[J].中国微侵袭神经外科杂志,2006,11(2):71-74.
作者姓名:王翀  朱贤立  赵洪洋  李玉  李金星  赵甲山
作者单位:华中科技大学同济医学院附属协和医院神经外科,湖北,武汉,430022
摘    要:目的探讨ICAM—1在大鼠弥漫性脑损伤中的表达及意义。方法采用Marmarou方法获得大鼠弥漫性脑损伤模型.实时定量RT—PCR、S—P免疫组化法分别测定ICAM—1蛋白和mRNA在外伤后不同时间点的表达变化.干湿重法测脑组织含水量.组织切片苏木精一伊红染色观测炎性细胞浸润情况。结果外伤组与假手术对照组比较,ICAM—1蛋白表达分别于伤后6h明显升高.72h达到高峰(P〈0.05),ICAM—ImRNA表达3h即明显升高,72h达最高峰,其后下降。7d时仍高于假手术对照组(P〈0.01)。伤后脑组织含水量较假手术对照组高,同时炎性细胞大量聚集。结论大鼠脑外伤诱导了ICAM—1的表达.ICAM—1通过介导炎性细胞的浸润可能参与了伤后脑水肿的形成过程.

关 键 词:脑损伤  胞间黏附分子1  逆转录聚合酶链反应  免疫组织化学  脑水肿
文章编号:1009-122X(2006)02-0071-04
收稿时间:2005-08-16
修稿时间:2005-10-18

Expression and significance of intercellular adhesion molecule-1 after diffuse brain injury in rats
WANG Chong, ZHU Xianli, ZHAO Hongyang, et al.Expression and significance of intercellular adhesion molecule-1 after diffuse brain injury in rats[J].Chinese Journal of Minimally Invasive Neurosurgery,2006,11(2):71-74.
Authors:WANG Chong  ZHU Xianli  ZHAO Hongyang  
Abstract:Objective To explore the expression and significance of ICAM-1 after diffuse brain injury in rats. Methods The rat models of diffuse brain injury were established by Marmarou's method. Real-time quantitative PCR, immunohistochemistry, dry-wet weight method, histological techniques and haematoxylin and eosin stain were used to detect expression of ICAM-1, the change of mRNA at different time phases, water containing in the brain tissue and the inflammatory infiltration respectively after diffuse brain injury. Results The expression of ICAM-1 markedly increased 6h after injury in the injury groups in contrast to sham-operated group, peaked at the 72nd hour (P<0.05). ICAM-1 mRNA expression in the injury group markedly increased at the 3rd hour, peaked at the 72nd hour and was higher than that in sham-operated group at the 7th days (P<0.01). The water containing in the brain tissue after brain injury in the injury group was higher than that in the sham-operated group with prominent inflammatory cell infiltration in the brain tissue. Conclusion Traumatic brain injury could induce expression of ICAM-1, suggesting that ICAM-1 may contribute to the formation of brain edema by inducing infiltration of inflammatory cells into traumatic brain tissue.
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