法医学杂志 ›› 2004, Vol. 0 ›› Issue (2): 65-67+1.

• 论文 •    下一篇

大鼠液压冲击脑损伤后bFGF及其受体FGFR1的表达

黄代新,张林,吴梅筠,陈于波,吴家马文   

  1. 华中科技大学同济医学院法医学系,四川大学华西基础医学与法医学院,四川大学华西基础医学与法医学院,四川大学华西基础医学与法医学院,四川大学华西基础医学与法医学院 湖北武汉430030 ,四川成都610041 ,四川成都610041 ,四川成都610041 ,四川成都610041
  • 发布日期:2004-04-25 出版日期:2004-04-28

The expression of bFGF and its receptor FGFR1 in rat after fluid-percussive brain injury

HUANG DAI-XIN1, ZHANG LIN2, WU MEI-YUN2, ET AL. (1.FACULTY OF FORENSIC MEDICINE, TONGJI MEDICAL COLLEGE, HUAZHONG UNIVERSITY OF SCIENCE AND TECHNOLOGY, WUHAN 430030, CHINA; 2. COLLEGE OF ELEMENTARY MEDICINE AND FORENSIC MEDICINE, SICHUAN UNIVERSITY, CHENG   

  • Online:2004-04-25 Published:2004-04-28

摘要: 目的观察脑损伤后碱性成纤维细胞生长因子(bFGF)及其受体FGFR1的表达及其时序性变化,探讨脑损伤的分子机制及法医学脑损伤时间推断。方法用免疫组织化学技术观察大鼠侧位中度液压冲击脑损伤后bFGF及FGFR1蛋白在伤后不同时间(30min,1,3,6,12h,1,3,7d)的表达情况,以正常大鼠及手术大鼠作为对照。结果正常对照组和手术对照组大鼠脑组织内有低水平的bFGF和FGFR1表达。脑冲击伤后6h,大脑皮层和脑干bFGF和FGFR1蛋白表达开始显著增加,1~3d达高峰,7d时已有所下降;海马冲击后3h即开始增加,1d达峰值,此后逐渐下降,7d时恢复正常。结论脑损伤可诱导bFGF/FGFR1的表达,提示机体对脑损伤存在自身保护机制,其表达的时序性改变可望用于法医学脑损伤时间推断。

关键词: 液压冲击脑损伤, 碱性成纤维细胞生长因子, 成纤维细胞生长因子受体

Abstract: Objective Study on the pattern of changes of bFGF and FGFR1 immunoreactivity occurred in the experimental brain injury model for the purpose of providing the scientific basis for molecular pathological diagnosis, forensic identification, clinical treatment as well as further ascertaining the molecular mechanism of brain injury. Methods Male SD rats were divided into normal control, sham operation control and injury groups. The rats of injury groups were subjected to moderate lateral fluid percussion brain injury (0.2 mPa). The injury groups were then subdivided into 30 min, 1,3,6,12 h,1,3,7 d groups according to the time elapsed after injury. The SP immunohistochemistry method was used to examine the expression of both bFGF and FGFR1 factors in rat brain. Results In the brain of normal control and sham operation control groups, the low expression levels of bFGF and FGFR1 were observed. The increase of bFGF and FGFR1 immunoreactivity could be observed 6 h after injury in cortex and brain stem, reached to the peak at 1 d and remained at the high level up to 3 d, then partly declined at 7 d. In hippocampus, however, the increase occur as early as 3 h after injury, reached to the peak at 1 d and then decreased progressively, and returned to basal level at 7 d. Conclusion The results suggested that brain injury induced the gene expressions of bFGF and FGFR1. The bFGF may contribute to maintenance of nerve cell survival and the repair of damaged neural tissues after CNS injury and the patterns of their level change were quite regular and can be used for timing of injury in forensic medicine aspect.

Key words: fluid percussion brain injury, basic fibroblast growth factor, fibroblast growth factor receptor