Effect of glucose regulated protein 78 on neuronal apoptosis after cerebral ischemia reperfusion injury in rats
10.3760/cma.j.issn.1006-7876.2009.11.015
- VernacularTitle:葡萄糖调节蛋白78对脑缺血再灌注后神经细胞凋亡的影响
- Author:
Yongbo ZHAO
;
Xiaoyan SONG
;
Xiaolin ZHOU
;
Yuncheng WU
;
Wenwen LIU
- Publication Type:Journal Article
- Keywords:
Brain ischemia;
Reperfusion injury;
Neurons;
Apoptosis
- From:
Chinese Journal of Neurology
2009;42(11):765-770
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of glucose regulated protein (GRP)78 on the neuronal apoptosis after cerebral ischemia reperfusion injury in rats. Methods Middle cerebral artery ischemia reperfusion rat's models were used with the modified filament method. The expression of GRP78 in the ischemic penumbra tissue was detected by RT-PCR, Western blot and immunohistochemistry at different time points. Primary cultured rat's neurons were exposed to hypoxia and subsequently reoxygenation. Western blot was used to investigate the expression of GRP78. The changes of the neuronal apoptosis after overexpression of GRP78 induced by 2-deoxyglucose were detected. Results The expression of GRP78 in the ischemic penumbra tissue in model group was significantly increased (mRNA : 0.7367±0.0651, F= 477.160, P < 0.01 ; Protein : 0. 8129±0. 0748, F=39.857, P < 0.01). The neuronal survival status was increased after overpression of GRP78 (increased by 39.22% ± 0. 44%, t=46.374, P < 0.01) while the neuronal apoptosis was decreased (decreased by 16.60±1.02, t=7.530, P <0.01). Conclusion Focal cerebral ischemia reperfusion can induce endoplasmic reticulum stress which plays a role in the neuronal apoptosis. The increased expression of GRP78 may protect the ischemic tissue from neuronal apoptosis.
