Effects of ischemic pre- and postconditioning on cerebral glycogen synthase kinase-3 beta activity in a rat model of cerebral ischemia-reperfusion
10.3760/cma.j.issn.0254-1416.2010.11.033
- VernacularTitle:缺血预处理和缺血后处理对大鼠脑缺血再灌注时糖原合酶激酶-3β活性的影响
- Author:
Bo ZHAO
;
Zhongyuan XIA
;
Wenwei GAO
;
Jiabao HOU
;
Yang WU
;
Hong GAO
;
Changjian WU
- Publication Type:Journal Article
- Keywords:
Ischemic preconditioning;
Glycogen synthase kinase 3;
Reperfusion injury;
Brain;
Ischemic postconditioning
- From:
Chinese Journal of Anesthesiology
2010;30(11):1391-1393
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of ischemic pre- and postconditioning on cerebral glycogen synthase kinase-3 beta (GSK-3β) activity in a rat model of global cerebral ischemia-reperfusion (I/R).Methods Forty male Wistar rats weighing 200-230 g were randomly allocated into 4 groups (n =10 each) : Ⅰ group sham operation (group S); Ⅱ group I/R; Ⅲ group ischemic preconditioning (group IPR) and Ⅳ group ischemic postconditioning (group IPO). The animals were anesthetized with intraperitoneal 10% chloral hydrate 0.4 ml/100 g. Global cerebral ischemia was induced by four-vessel-occlusion in group Ⅱ , Ⅲ and Ⅳ. Bilateral vertebral arteries were cauterized and bilateral carotid arteries were occluded for 10 min. In group IPR cerebral ischemia was preceded by 3 cycles of 10 s ischemia followed by 30 s reperfusion. The group IPO received 3 cycles of 30 s reperfusion followed by 10 s ischemia at the end of 10 min cerebral ischemia. The animals were killed 2 days later. The brains were immediately removed for determination of neuronal apoptosis in the cortex (by TUNEL), the infarct size (by TTC), p-GSK-3β activity (by spectrum assay) and the expression of Bcl-2, Bax and Caspase-3 (by SP). Linear correlation of p-GSK-3β activity with the number of apoptotic neurons in the cortex and cerebral infarct size was analyzed. Results Cerebral I/R significantly increased the number of apoptotic neurons in the cortex and infarct size, decreased p-GSK-3β activity, down-regulated Bcl-2 expression and up-regulated Bax and Caspase-3 expression in group I/R as compared with group S. Ischemic pre- and postconditioning significantly attenuated these cerebral I/R-induced changes. The p-GSK-3β activity was negatively correlated with the number of apoptotic neurons in the cortex and cerebral infarct size. Conclusion Ischemic pre- and postconditioning reduces cerebral I/R injury through inhibiting the activity of GSK-3β.
