Effect of ischemic preconditioning on the expression of glial fibrillary acidic protein after ischemia-reperfusion in rats
10.3760/cma.j.issn.1673-4165.2010.09.006
- VernacularTitle:缺血预处理对脑缺血再灌注大鼠脑组织胶质纤维酸性蛋白表达的影响
- Author:
Yuman HAO
;
Zuming LUO
;
Dong ZHOU
;
Li GAO
;
Zhong ZENG
;
Zhong ZHANG
;
Yan LIU
- Publication Type:Journal Article
- Keywords:
Ischemic Preconditioning;
Brain ischemia;
Glial fibrillary acidic protein;
Astrocytes;
Disease models,animal;
Rats
- From:
International Journal of Cerebrovascular Diseases
2010;18(9):664-667
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of focal cerebral ischemic preconditioning on the expression of glial fibrillary acidic protein (GFAP) and to investigate the significance of astrocyte activation in cerebral ischemic tolerance.Methods Thirty-six healthy male SpragueDawley rats were randomly divided into reischenmic,ischemic and control groups (n = 12 in each group) after ischemic preconditioning.The former two groups received 10 minutes middle cerebral artery occlusion (MCAO) preconditioning or sham operation 3 days before the 2-hour MCAO.The rats were killed 24 hours after the second MCAO.The control group only receivedthe two sham operations with an interval of three days.The infarct volume,histopathological changes,and GFAP expression in each group were compared.Results The infarct volume after ischemic preconditioning in the reischenmic and ischemic groups was 136.85 ± 14.51 mm3and 281.37 ± 29.93 mm3 respectively.The former was significantly reduced 53.15%compared to the latter (P =0.007).At the same time,neuronal degeneration and necrosis was reduced significantly,and GFAP expression was upregulated significantly (the mean absorbance for immunohistochemical staining in both groups was 102.66 ± 8.39 and 86.28 ± 6.19respectively,P = 0.009) after ischemic preconditioning in the reischemic group.Conclusions Focal ischemic preconditioning may induce brain ischemic tolerance and promote GFAP expression.The activation of astrocytes may be one of the mechanisms of cerebral ischemic tolerance.
