全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

糖尿病脑缺血再灌注大鼠海马胶质细胞凋亡研究

, PP. 477-480

Keywords: 脑缺血,再灌注,糖尿病,高血糖,神经胶质细胞,细胞外信号调节激酶1/2,大鼠

Full-Text   Cite this paper   Add to My Lib

Abstract:

目的探讨糖尿病脑缺血再灌注时神经胶质细胞损伤加重的分子机制。方法96只成年SD大鼠随机分为4组假手术对照组、正常血糖脑缺血组、糖尿病脑缺血组、PD98059预防糖尿病脑缺血组,每组24只。采用链脲佐菌素诱导糖尿病,双血管闭塞联合放血法建立糖尿病大鼠全脑缺血模型,运用HE染色、TUNEL方法,研究高血糖状态下脑缺血再灌注时和使用P-ERK1/2阻断剂PD98059后海马CA4、CA2神经胶质细胞的凋亡表达状况。结果糖尿病大鼠全脑缺血再灌注时,海马CA4、CA2区神经胶质细胞在缺血15min,再灌注1、3h凋亡细胞数量增加,高于正常血糖脑缺血组大鼠(P<0.05),使用P-ERK1/2阻断剂PD98059后,在缺血再灌注各时间点神经胶质细胞的凋亡细胞表达减少,低于糖尿病脑缺血组(P<0.05)。结论高血糖加重脑缺血再灌注时神经胶质细胞的损伤,高血糖诱导的ERK1/2磷酸化可能介导了神经胶质细胞的凋亡。

References

[1]  Astrup J, Siesjo BK, Symon L.Thresholds in cerebral ischemia-the ischemic penumbra[J]. Stroke,1981,12:723.
[2]  Mc Donald JW, Althomsons SP, Hyrc KL, et al. Oligodendrocytes from forebrain are highly vulnerable to AMPA/kainite receptor-me-diated excitotoxity[J]. Nat Med, 1998,4(3):291-297.
[3]  Cavallini A, MicieliG, MarcheselliS, et al. Role of monitoring in management of acute ischemic stroke patients[J]. Stroke,2003,34(11): 2599-2603.
[4]  Li PA, He QP, Yi-Bing, et al. Phosphorylation of extracellular signal-regulated kinase after transient cerebral ischemia in hyperglycemic rats [J]. Neurobiol Dis, 2001,8(1): 127-35.
[5]  张建中,景丽. 磷酸化细胞外信号调节蛋白激酶加重糖尿病大鼠脑缺血性损伤[J]. 第三军医大学学报,2007,24:2339-2342.
[6]  Murray B, Alessandrini A, Cole AJ. Inhibition of the p44/42 MAP kinase pathway protects hippocampal neurons in a cell-culture model of seizure activity[J]. Proc Natl Acad Sci USA,1998,95:11975-11980.
[7]  Hu BR, Liu CL, Park DL. Alteration of MAP kinase pathways after transient forebrain ischemia[J]. Cereb Blood Flow Metab, 2000,20(7):1089-1095.
[8]  Namura S, Iihara K, Takama S, et al. Intravenous administration of MEK inhibitor U0126 affords brain protection against forebain ischemia and focal cerebal ischemia[J]. Proc Natl Acad Sci USA, 2001,98:11569-11574.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133