摘要
目的观察大鼠颅脑损伤后脑组织中Bcl-2、Bax表达和血清一氧化氮(NO)、超氧化物歧化酶(SOD)的变化,探讨大鼠颅脑损伤后神经细胞凋亡机制。方法选用大鼠48只,按时间段随机分为8组,采用自由落体法建立大鼠脑损伤模型,分别于伤后2、6、12、24、48小时及7、14天采取血清,制备脑组织切片,采用TUNEL法检测神经细胞凋亡,用免疫组织化学方法检测Bcl-2、Bax,并测定血清中NO含量和SOD活性。结果颅脑损伤后,TUNEL(+)细胞和Bcl-2、Bax表达均明显升高,分别在伤后12、48小时达到高峰;NO含量迅速上升,12小时达到高峰;而SOD降低,48小时达最低点,随着时间的延长,各值均逐步恢复至对照组水平。结论颅脑损伤后,NO可促使Bcl-2、Bax表达升高,但对Bax的影响更明显,引起细胞凋亡。相反,SOD降低了Bcl-2、Bax表达,抑制了细胞的凋亡。颅脑损伤后SOD的降低也是引起细胞凋亡的主要因素。
Objective To investigate the changes of NO,SOD and Bcl-2,Bax expression after traumatic brain injury（TBI） in rats. Methods Forty-eight rats were randomly divided into 8 groups, the experimental TBI model was established by Feeney＇s method. The brain tissue and serum sample were taken 2,6,12,24 and 48h and 7,14d after TBI. Apoptosis of cells was detected by TUNEL, Bcl-2/ Bax expression were inspected by immunochemical method. The quantity of NO and enzymatic activity of SOD in serum were determined. Results The number of TUNEL（＋ ） cell and Bcl-2,Bax immunopositive cell were all increased significantly,which reached their highest points at 12,48h respectively. NO increased to its highest point at 12h after TBI,while activity of SOD decreased and arrived its lowest point at 48h after TBI. Then both of which slowly returned the level of the control group. Conclusion The more quantity of NO produced after TBI enhanced Bcl-2 and Bax expression ,the effects of which on Bax is more obvious,leading to cell apoptosis. The lower quantity of SOD reduced Bcl-2 and Bax expression and inhibited apoptosis. The decreased SOD after TBI played an important role in apoptotsis of brain cells.
出处
《创伤外科杂志》
2006年第3期238-240,共3页
Journal of Traumatic Surgery
