Citation

Huang DX, Zhang L, Wu MY. Fa Yi Xue Za Zhi 2004; 20(2): 65-67.

Affiliation

Faculty of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. huangdaixin@mails.tjmu.edu.cn

Copyright

(Copyright © 2004, Si fa bu Si fa jian ding ke xue ji shu yan jiu suo)

DOI

unavailable

PMID

15311515

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.

Language: zh