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脑缺血再灌注后ICE、Bcl-2的表达及丹参的神经保护作用研究
引用本文:张金涛,赵书平,王树新,王利群,李义召,刘赛男. 脑缺血再灌注后ICE、Bcl-2的表达及丹参的神经保护作用研究[J]. 卒中与神经疾病, 2001, 8(1): 26-28
作者姓名:张金涛  赵书平  王树新  王利群  李义召  刘赛男
作者单位:1. 山东泰安市,中国人民解放军第88医院神经内科 271000
2. 山东医科大学
摘    要:目的观察凋亡相关基因白介素-lβ转化酶(ICE)、Bcl-2在脑缺血后的表达情况以及丹参(RSM)对其影响。方法健康沙土鼠63只,随机分成三组假手术组、对照组和丹参组。采用沙土鼠前脑缺血再灌注模型,在沙土鼠脑缺血再灌注后的2h、6h、12h、1d、3d、5d及7d分别处死沙土鼠,将脑组织进行免疫组织化学染色观察。结果ICE的蛋白表达主要在海马CA1区、CA4区及皮质,免疫阳性细胞呈褐色,第3天达高峰,第5天后减少;丹参组ICE的蛋白表达明显减少(P<0.01)。Bcl~2的蛋白表达主要在大脑皮层、纹状体、丘脑及海马等广泛区域,并于6h达高峰,其后减少;丹参组Bcl-2的蛋白表达明显增加,特别是在海马CA1区及大脑皮层区(P<0.01)。结论ICE在调节脑缺血中可能发挥重要作用;Bcl-2主要通过抑制细胞凋亡的早期环节而发挥作用;丹参能下调脑缺血后的ICE表达、上调脑缺血后的Bcl-2表达进而发挥其神经保护作用。

关 键 词:脑缺血白介素-1β转化酶(ICE)Bcl-2基因表达丹参
文章编号:1007-0478(2001)01-0026-03
修稿时间:2000-04-25

Study of RSM
Zhang Jintao,Li Yizhao,Zhao Shuping,et al.. Study of RSM[J]. Stroke and Nervous Diseases, 2001, 8(1): 26-28
Authors:Zhang Jintao  Li Yizhao  Zhao Shuping  et al.
Affiliation:Zhang Jintao,Li Yizhao,Zhao Shuping,et al. Department of Neurology,The 88th Hospital of PLA,Taian 271000
Abstract:Objective To study the expression of ICE、Bcl - 2 after ischemiaand reperfusion and to study the effects of Radix Salviae Miltiorrhizae(RSM) on them. Methods 63 gerbils were divided into three groups(sham -operated group, control group and RSM group), and decapitation were operated on gerbils at 2h、6h、 12h、 ld 、3d、 5d、7d after ischemia and reperfusion. Immediately, using immunohistochemical technique, we observed the expression of Interleukin-1 β converting enzyme(ICE), Bcl-2 and the effects of RSM on them. Results Expression of ICE were observed markedly in CAi ,CA4 and cortex and the neurons were in brown with the peak at 3rd day and decreasing at 5th day after ischemia and reperfusion. Bcl-2 were markedly induced in cortex, stria body, thalamencephalon and hippocampus with the peak at 6h. We also found that expression of ICE were down-regulated and that of Bcl-2 were up-regulated in RSM group(P<0.01). Conclusion Our results indicate that ICE may play an important role in regulating ischemic reperfusion, Bcl-2 may restrain apoptosis at the early phase and RSM may ameliorat ischemic damage by reducing the apoptosis through regulating ICE and Bcl-2.
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