氯化锂对脑缺血预处理后PI3K/AKT/GSK3β通路的影响机制

被引：8

作者：

张慧

姜咏梅

尹琳

机构：

[1] 大连医科大学附属二院神经内科

来源：

中国医药导报 | 2011年 / 8卷 / 24期

关键词：

脑缺血预处理; PI3K/AKT; GSK-3β; Mcl-1; 氯化锂;

D O I：

暂无

中图分类号：

R743.31 [短暂性脑缺血];

学科分类号：

1002 ;

摘要：

目的:研究脑缺血预处理(CIPC)中氯化锂对PI3K/AKT/GSK3β信号通路调节变化及影响。方法:制作脑缺血、CIPC及氯化锂干预模型,进行神经功能缺损评分;TTC法脑组织染色计算脑梗死体积;应用Western blotting检测AKT、p-AKT、GSK-3β、p-GSK-3β(ser9)、Mcl-1的蛋白表达。结果:与脑缺血组比较,氯化锂组及CIPC组p-AKT、Mcl-1、p-GSK-3β(ser9)的蛋白表达均增高,神经功能缺损评分及脑梗死体积降低(P<0.05);与CIPC组比较,氯化锂组进一步提高了p-AKT、Mcl-1、p-GSK-3β(ser9)的蛋白表达、降低了神经功能缺损评分及脑梗死体积(P<0.05)。结论:脑缺血预处理增高p-GSK-3β(ser9)表达,增加p-AKT、Mcl-1的表达。氯化锂可加强脑缺血预处理的这一神经保护作用。

引用

页码：22 / 25

页数：4

共 8 条

[1] 脑缺血预处理大鼠脑IL-6和Ngb的表达及尤瑞克林对其表达的干预 [J].

姜长斌 ;

丁聪 ;

尹琳 .

中国神经免疫学和神经病学杂志, 2009, 16 (01) :42-46

[2]

Role of PI3-K/Akt pathway and its effect on glial cell line-derived neurotrophic factor in midbrain dopamine cells[J]. Hong-jun WANG Jun-ping CAO Jing-kao YU Dian-shuai GAO~2 Research Centre of Neurobiology,Xuzhou Medical College,Xuzhou 221002,China.Acta Pharmacologica Sinica. 2007(02)

[3]

Regulation of Akt mRNA and protein levels by glycogen synthase kinase-3β in adrenal chromaffin cells: Effects of LiCl and SB216763[J] . Takayuki Nemoto,Tasuku Kanai,Toshihiko Yanagita,Shinya Satoh,Toyoaki Maruta,Norie Yoshikawa,Hideyuki Kobayashi,Akihiko Wada.European Journal of Pharmacology . 2008 (1)

[4] Inhibition of GSK-3 reduces infarct volume and improves neurobehavioral functions [J].

Koh, Seong-Ho ;

Yoo, A. Rum ;

Chang, Dae-Il ;

Hwang, Se J. ;

Kim, Seung H. .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2008, 371 (04) :894-899

[5] Preconditioning suppresses inflammation in neonatal hypoxic ischemia via Akt activation [J].

Yin, Wei ;

Signore, Armando P. ;

Iwai, Masanori ;

Cao, Guodong ;

Gao, Yanqin ;

Johnnides, Michael J. ;

Hickey, Robert W. ;

Chen, Jun .

STROKE, 2007, 38 (03) :1017-1024

[6] Evidence of phosphorylation of Akt and neuronal survival after transient focal cerebral ischemia in mice [J].

Noshita, N ;

Lewén, A ;

Sugawara, T ;

Chan, PH .

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2001, 21 (12) :1442-1450

[7] Rapid preconditioning protects rats against ischemic neuronal damage after 3 but not 7 days of reperfusion following global cerebral ischemia [J].

PerezPinzon, MA ;

Xu, GP ;

Dietrich, WD ;

Rosenthal, M ;

Sick, TJ .

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1997, 17 (02) :175-182

[8]

Phosphatidylinositol-3-kinase/Akt/glycogen synthase kinase-3 beta and ERK1/2 pathways mediate protective effects of acylated and unacylated ghrelin against oxygen-glucose deprivation-induced apoptosis in primary rat cortical neuronal cells. Chung H,Seo S,Moon M, et al. The Journal of Endocrinology . 2008

← 1 →