摘要
目的:观察Bcl-2蛋白在前脑缺血再灌注后细胞凋亡中的变化,探讨脑缺血再灌注后细胞凋亡的分子机制。方法:21只雄性SD大鼠随机分为7组,即对照组,脑缺血再灌注后1、3、6、12、24、48h组。大鼠断头处死后,解剖取材,固定、包埋、切片。用原位末端标记法(TUNEL)检测前脑缺血再灌注模型海马的细胞凋亡情况,用免疫组化方法检测相关基因Bcl-2表达的变化。结果:前脑缺血再灌注1、3h海马区未见凋亡细胞出现,6h开始出现,24h达高峰,之后开始下降。Bcl-2阳性表达在前脑缺血再灌注1h即出现,12h达高峰,之后下降至低水平。结论:Bcl-2蛋白表达在海马神经元凋亡过程中起重要作用。
Objective To observe the changes of Bcl-2 expression in apoptosis of neurons and to investigate the molecular mechanism of apoptosis following forebrain cerebral ischemia-reperfusion. Methods Twenty-one male SD rats were randomly divided into 7 groups: control group, 1,3,6,12,24,48 h after focal cerebral ischemia-reperfusion group. The neuronal apoptosis in the hippocampus after forebrain ischemia-reperfusion was detected by terminal deoxynuleotide transferase-mediated dUTP nick end labeling (TUNEL) technique and the changes in Bcl-2 expression were determined using immunohistochemical method. Results The apoptotic cells in the hippocampus appeared at 6 h after forebrain ischemia-reperfusion, peaked at 24 h, and then decreased. Bcl-2 gene was positively expressed at 1 h and the expression reached its peak level at 12 h, and then declined to a lower level. Conclusion The expression of Bcl-2 protein plays a vital role in the process of neuronal apoptosis.
出处
《实用医学杂志》
CAS
2007年第20期3169-3170,共2页
The Journal of Practical Medicine