Expression of extracellular signal-regulated kinase 1/2 and neuronal apoptosis in hippocampal CA4 region after cerebral ischemia-reperfusion in diabetic rats
10.3760/cma.j.issn.1673-4165.2009.08.003
- VernacularTitle:糖尿病大鼠脑缺血再灌注后细胞外信号调节激酶1/2表达与海马CA4区神经元凋亡
- Author:
Yi MA
;
Li JING
;
Fengying GUO
;
Jianzhong ZHANG
- Publication Type:Journal Article
- Keywords:
diabetes mellitus;
cerebral ischemia;
reperfusion injury;
mitogen-activatedprotein kinase 1;
apoptosis;
rats
- From:
International Journal of Cerebrovascular Diseases
2009;17(8):573-576
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression of neuronal extracellular signal-regulated kinase 1/2 (ERK1/2) and its significance after cerebral isehemia reperfusion in diabetic rats. Methods Seventy-two healthy adult SD rats were randomly divided into sham-operation, normal glucose with cerebral ischemia and diabetes with cerebral ischemia groups. Each group was redivided into ischemia 15 minutes and reperfusion 1, 3 and 6 h subgroups according to the different time points of ischemia reperfusion (n = 6 in each subgroup). Streptozocin was used to induce diabetes, and a global cerebral ischemia model of diabetic rat was established by the bilateral vascular occlusion combining with bloodletting, TUNEL and immunohistochemistry were used to observe neuronal apoptosis and the expression of the phosphorylation of ERK1/2 in hippocampal CA4 region. Results The incidences of neuronal apoptosis in hippocampal CA4 region for ischemia 15 minutes and reperfusion 1, 3 and 6 h in the diabetes with cerebral ischemia group were significantly higher than those in the normal glucose with cerebral ischemia group (P < 0. 05); the expressions of the phosphorylation of ERK1/2 at all time points in the diabetes with cerebral ischemia group were higher, and reperfusion 1 and 3 h were significantly higher than those in the normal glucose with cerebral ischemia group (P < 0.01). Conclusions ERK1/2 might involved in the mechanism of neuronal injury after diabetes aggravating cerebral ischemia-reperfusion.
