The expression of XIAP, Smac, HtrA2 and XAF1 in the rat hippocampus following status epilepticus
- VernacularTitle:大鼠癫(癎)持续状态后海马内X-连锁凋亡抑制蛋白及其负性调控因子的表达
- Author:
Shuyu LI
;
Bo XIAO
;
Fangfang BI
;
Yanhui ZHOU
;
Xiaoqin LU
;
Xiaomei WU
- Publication Type:Journal Article
- Keywords:
Status epilepticus;
Hippocampus;
X-linked inhibitor of apoptosis proteins;
Carrier proteins;
Mitochondrial proteins;
Serine endo peptidases
- From:
Chinese Journal of Neurology
2008;41(9):594-597
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression of XIAP, Smac, HtrA2 and XAF1 in the hippocampus following SE in rats and to explore the pathophysiological mechanisms of expression of XIAP and its negative regulators after SE. Methods The lithium-pilocapine model of status epilepticus was established in SD rat. XIAP, Smac, HtrA2, XAF1 and activated caspase-3 protein were examined using immunohistochemistry. Western blot was used to detect the protein levels of XIAP, Smac, HtrA2 and activated easpase-3. Results XIAP immunoreactivity diffusely distributed within the neuron after SE. Compared with the control group, the expression of CA3 XIAP protein in the SE group was increased gradually since 2 hours (0.5503±0.0172 vs 0.1507±0.0165, t=115.87, P<0.01), peaking at 8 hours (0.6221±0.0238 vs 0.1507±0.0165, t=136.69, P<0.01). The expression of CA3 Smac, HtrA2, XAF1 and activated caspase-3 protein were increased generally following SE. Western blot analysis showed a significant increase in Stoat, HtrA2, activated caspase-3 protein levels from 2 to 72 hours following SE, but no significant differences were seen in XIAP protein levels between the control group and the SE group. Conclusions The XIAP, Smac, HtrA2 and XAF1 are involved in the regulation of neuronal apoptosis and implicated in pathophysiological mechanisms of neuronal damage after SE.
