Expression of procaspase-3 in the mouse hippocampus after transient forebrain ischemia
- VernacularTitle:小鼠短暂前脑缺血海马区半胱氨酸天冬氨酸蛋白酶3酶原表达形式的变化
- Author:
Tianhui LIU
;
Rui CHEN
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2005;9(32):225-227
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:After cerebral ischemia/reperfusion injury,as a executioner caspase, procaspase-3 and caspase-3-like activity increased significantly. We observe both the dephosphorylated and phosphorylated procaspase-3, and try to find out their variations during the processes of cerebral ischemia/reperfusion injury.OBJECTIVE:Observe the expression of procaspase-3 in hippocampus following transient forebrain ischemia.DESIGN: A randomized and controlled experiment.DEPARTMENT:Department of Biochemistry and Molecular Biology,Capital University of Medical Sciences.SETTING:Department of Hyperbaric Oxygen of Beijing Chaoyang Hospital Affiliated to Capital University of Medical Sciences.METHODS:Transient forebrain ischemia was induced by bilateral common carotid occlusion (BCCAO) for 20 minutes. Hippocampus was obtained at reperfusion time points of 6 hours, 12 hours,24 hours and 48 hours respec-tively after 20 minutes of BCCAO. Sham-operated group did not occlude bi-lateral common carotid, and hippocampus was obtained at reperfusion time point of 24 hours. Western Blotting was used to detect the level of procaspase-3.MAIN OUTCOME MEASURES:The comparison of total procaspase-3,dephosphorylated procaspase-3 and phosphorylated procaspase-3 level in hippocampus between each group.3 level: Total procaspase-3 level increased in hippocampus at reperfusion time points of 12 hours and 24 hours post-BCCAO (9 133.1 ±2 216.3,dephosphorylated procaspase-3 level increased in hippocampus at reperfusion time point of 24 hours post-BCCAO (7812.0±1625.1, 3825.8±155.6, P was not significant (P ＞ 0.05) as compared with the expression levels in sham-operated mice.CONCLUSION: Procaspase-3 is upregulated after ischemia/reperfusion.The increment of dephosphorylated form of procaspase-3 was higher than that of phosphorylated form of procaspase-3 upon cerebral ischemia/reperfusion injury, which indicates that cerebral ischemia/reperfusion injury possibly induced the dephosphorylation of procaspase-3 and promoted its transforming into activated form.
