Changes of the expressions of endoplasmic reticulum chaperones GRP78 and caspase-9 and-12 in fetal rats with intrauterine distress
- VernacularTitle:宫内窘迫胎鼠脑组织葡萄糖调节蛋白78及胱冬酶9,12表达的改变
- Author:
Zeyan ZHAO
;
Jianhua ZHANG
;
Hua ZHANG
- Publication Type:Journal Article
- Keywords:
Intrauterine distress;
Fetal rat;
Endoplasmic reticulum chaperone;
Caspase
- From:
Journal of Medical Postgraduates
2003;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of glucose-regulated protein 78(GRP78) and caspase-9 and-12 in intrauterine distress-induced hypoxic-ischemic cerebral damage in fetal rats.Methods:The fetal rat model of intrauterine distress was constructed and the fetal rats were randomly divided into a normal,a sham operation and an ischemia-reperfusion(IR) group.Neuron apoptosis was analyzed by in situ end-labeled DNA(TUNEL).The expressions of caspase-9 and-12 and GRP78 proteins in the hippocampus CA1 area were detected by immunohistochemical staining.Results:Ischemia-reperfusion damage induced classic neuron apoptosis and the number of the apoptotic neurons in the hippocampus CA1 area increased with the progression of reperfusion.The expressions of GRP78 and caspase-9 and-12 were weak in the normal and sham operation group.In the IR group,the expression of GRP78 reached the peak value 3 hours after the reperfusion and then decreased gradually;the intensity of caspase-12 was increased rapidly while that of caspase-9 elevated very little within 3 hours,but both reached the peak value at 12 hours.Conclusion:Intrauterine distress-induced hypoxic-ischemic cerebral damage in fetal rats may trigger the homeostatic control system in the endoplasmic reticulum through the increased expression of GRP78.The apoptotic pathway mediated by caspase-12 in the endoplasmic reticulum may be one of the mechanisms underlying cerebral ischemic injury.
