Effects of ischemic preconditioning on the expression of extracellular signal-regulated protein kinase and c-jun N-terminal kinase in hippocampus in a gerbil model of cerebral ischemia-reperfusion injury
- VernacularTitle:缺血预处理对脑缺血再灌注损伤沙土鼠海马细胞外信号调节激酶和c-jun氨基末端激酶表达的影响
- Author:
Yao-Qi WANG
;
Jun LI
;
Yue-Ping WANG
;
Hong CAO
;
Guangming LI
;
Yinming ZENG
- Publication Type:Journal Article
- Keywords:
Ischemic preconditioning;
Brain ischemia;
Reperfusion injurv;
Mitogen-activated protein kinase;
Phosphotranserase
- From:
Chinese Journal of Anesthesiology
1994;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of ischemic preconditioning (IP) on the expression of extracellular signal-regulated protein kinase (ERK) and c-jun N-terminal kinase (JNK) in hippocampus in a gerbil model of ischemia-reperfusion (I/R) injury and the role of ERK and JNK in the mechanism of ischemic cerebral preconditioning. Methods Gerbils of both sexes weighing 50-70kg were randomly divided into 4 groups : ( Ⅰ ) sham operation group; ( Ⅱ ) IP group; (Ⅲ) I/R group and ( Ⅳ ) IP + I/R group. Cerebral ischemia was produced by occlusion of bilateral common carotid arteries and confirmed by isoelectricity on EEG. In sham operation group bilateral common carotid arteries were exposed but not occluded. In IP and I/R groups the animals were subjected to 3 min (IP group) or 5 min (I/R group) cerebral ischemia respectively. In IP + I/R group the animals first underwent 3 min cerebral ischemia followed by 24h reperfusion and then were again subjected to 5 min cerebral ischemia. Open field test was performed to evaluate the behavioral deficit 1,3,5 and 7 days after ischemia. The animals were sacrificed at 15 min, 2, 4, 6h and 1, 3, 5, 7 days after ischemia. The brains were immediately removed for detection of apoptosis (TUNEL) and expression of p-ERK and JNK (immuno-histochemistry) in hippocampal CA1 and CA3 regions and microscopic examination. Results Compared with I/R group the behavioral deficit was significantly decreased and the number of living pyramidal neurons was significantly increased and apoptotic neurons significantly decreased in IP + I/R group. No p-ERK expression was detected in CA1 region in all of the 4 groups but in CA3 region the p-ERK expression was significantly higher in group IP + I/R than in group I/R. The p-JNK expression increased gradually during reperfusion in both CA1 and CA3 regions and was still detectable 7 days after ischemia and was significantly lower in CA1 region in group IP + I/R than in group I/R.Conclusion IP protects hippocampal neurons from I/R injury by inhibiting the expression of p-JNK in CA1 region and enhancing the activity of p-ERK in CA3 region
