摘要
目的探讨血管性痴呆(VD)大鼠海马CA1区凋亡相关蛋白Bcl-2和Bax的表达。方法将100只大鼠按随机数字法分为假手术组(Sham组)、血管性痴呆模型组(VD组),每组又分为1周、2周、4周、8周和12周5个不同观察时点(n=10)。采用四血管阻断法制备血管性痴呆模型,应用Morris水迷宫实验检测大鼠的学习记忆能力,TUNEL检测细胞凋亡,免疫组化法(SP法)检测凋亡相关蛋白Bcl-2和Bax的表达及两者之间的相关性。结果 (1)与Sham组比较,VD组大鼠海马CA1区Bcl-2、Bax阳性表达在1周开始增多,4周达到高峰,8周开始下降,到12周仍较高,差异均有统计学意义(P<0.05或<0.01)。(2)与Sham组比较,VD组大鼠海马CA1区不同时间点凋亡阳性细胞数明显增多,差异有统计学意义(P<0.05或<0.01);(3)相关性分析表明,血管性痴呆大鼠海马CA1区凋亡细胞数与Bcl-2及Bax蛋白表达呈正相关(r=0.845,P=0.000;r=0.866,P=0.000)。结论凋亡相关蛋白Bcl-2和Bax共同参与了血管性痴呆大鼠海马CAl神经细胞凋亡的调控。
Objective To observe the expression of Bcl-2 and Bax in CA1 area of hippocampus of vascular dementia rats.Methods One hundred mice were randomly divided into sham operation group(Sham group) and vascular dementia model group(VD group).Each group were divided randomly into 1,2,4,8 and 12 week time point groups(n =10).VD groups were established by blocking four vessels.Learning and memory abilities were detected by Morris water maze.Apoplotic cells were detected by TUNEL.The expression of Bcl-2 and Bax were detected by immunohistochemistry.Results(1) Compared to Sham group,apoptotic cells were increased at different time point of VD group in CA1 area of hippocampus of rats, there were statistical significance(P 0.05 or P 0.01).(2) The positive expression of Bcl-2 and Bax were raised at 1 week,peaked at 4 week,at 8 week began to decline,to 12 week still higher in VD group in CA1 area of hippocampus of rats, there were statistical significance(P 0.05 or P 0.01).(3) Correlation analysis showed that vascular dementia rat hippocampal CA1 region of apoptotic cells and Bcl-2 and Bax protein expression was positively correlated(r = 0.845,P = 0.000; r =0.866,P =0.000).Conclusion Apoptosis related protein Bcl-2 and Bax participated to regulate apoptosis together in hippocampal CA1 area of vascular dementia rats.
出处
《疑难病杂志》
CAS
2013年第9期709-711,F0003,共4页
Chinese Journal of Difficult and Complicated Cases
基金
唐山市科技攻关计划应用项目(No.121302110a)