Effects of preconditioning on tight junction and cell adhesion of cerebral endothelial cells

被引:15
作者
An, Ping [1 ]
Xue, Yi-Xue [1 ]
机构
[1] China Med Univ, Coll Basic Med, Dept Neurobiol, Shenyang 110001, Peoples R China
关键词
Preconditioning; Oxygen glucose deprivation; Blood-brain barrier; Tight junction; Cell adhesion molecules; BLOOD-BRAIN-BARRIER; NF-KAPPA-B; ISCHEMIA; INFLAMMATION; EDEMA; PATHOPHYSIOLOGY; REOXYGENATION; PERMEABILITY; MECHANISMS; EXPRESSION;
D O I
10.1016/j.brainres.2009.03.031
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Brain ischemia can usually disrupt the blood-brain barrier (BBB), increasing the permeability of BBB. Ischemic preconditioning could not only reduce neurons damage, but also protect the functions of BBB during brain ischemia. In this study, we used BBB model in vitro to examine the effects of preconditioning on cell viability, BBB permeability, tight junction and cell adhesion of rat brain microvascular endothelial cells (BMECs). The rat BMECs were exposed to 2.5 h of oxygen glucose deprivation (OGD) following 3 h of reoxygenation to simulate ischemia/reperfusion in vivo, using 0.5 h OGD as preconditioning. Results showed that OGD/reoxygenation induced cell death, increased BBB permeability, changed the distribution of endothelial cells tight junction protein ZO-1 and cellular framework protein F-actin, and increased the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). OGD preconditioning could partially protect cell viability and BBB permeability, maintain the membrane location of ZO-1 and F-actin, and decrease the expression of ICAM-1 and VCAM-1. Our study suggests that OGD preconditioning could stabilize the tight junction protein and alleviate cell adhesion to protect BBB function during ischemic stress. (C) 2009 Published by Elsevier B.V.
引用
收藏
页码:81 / 88
页数:8
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