Astrocytic response in the rodent model of global cerebral ischemia and during reperfusion

被引:19
|
作者
Sulkowski, G
Bubko, I
Struzynska, L
Januszewski, S
Walski, M
Rafalowska, U
机构
[1] Polish Acad Sci, Med Res Ctr, Dept Neurochem, Lab Pathobiochem Cent Nervous Syst, PL-02106 Warsaw, Poland
[2] Polish Acad Sci, Med Res Ctr, Lab Expt Nucl Med, PL-02106 Warsaw, Poland
[3] Polish Acad Sci, Med Res Ctr, Lab Ultrastruct Cell, PL-02106 Warsaw, Poland
关键词
global ischemia; reperfusion; free radicals; GFAP; glutathione; astrocytes;
D O I
10.1078/0940-2993-00229
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
The present study investigated alterations in astrocytic cells after global cerebral ischemia resulting from cardiac arrest immediately and at several intervals after reperfusion when excessive formation of highly cytotoxic free radicals is known to occur. The cellular fraction of astrocytic origin (glial plasmalemmal vesicles - GPV) was examined by biochemical and immunochemical procedures. A tendency towards an elevation in immunocontent of glial fibrillary acidic protein (GFAP) was noticed after 24 hours whereas a significant increase was observed 7 days post ischemic event. The features of astrocytic stimulation were also observed in electron microscopy studies. An enhanced amount of gliofilaments was noticed in brain sections obtained from rats after 7 days of recovery. Simultaneously, a gradual decrease of total glutathione level, depending on the duration of reperfusion, was observed in brain homogenates and in fractions of astroglial origin. The most considerable reduction was observed on day 1 (52%) and day 7 (65%) after reperfusion in brain homogenates and on day 7 (47%) in GPV fraction. The results indicate an enhanced reactivity of astrocytic cells in ischemic conditions concomitantly with a long lasting decrease of total glutathione. Obviously, the inability of astrocytic glutathione system to detoxify free radicals formed during ischemic/reoxidation conditions may lead to damage to cerebral neurons by oxidative stress.
引用
收藏
页码:31 / 38
页数:8
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