Dexamethasone enhances adenosine 5′-triphosphate-sensitive potassium channel expression in the blood-brain tumor barrier in a rat brain tumor model

被引:20
|
作者
Gu, Yan-ting [1 ]
Zhang, Hua [1 ]
Xue, Yi-xue [1 ]
机构
[1] China Med Univ, Coll Basic Med, Dept Neurobiol, Shenyang 110001, Liaoning, Peoples R China
基金
中国国家自然科学基金;
关键词
dexamethasone; bradykinin; blood-tumor barrier; blood-brain barrier; ATP-sensitive potassium channel; glioma; PERMEABILITY INCREASE; CELL-PROLIFERATION; SMOOTH-MUSCLE; K+ CHANNELS; GLUCOCORTICOIDS; MECHANISM; HYPOXIA;
D O I
10.1016/j.brainres.2007.05.053
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
This study was performed to determine whether dexamethasone (DEX) had an effect on ATP-sensitive potassium channels (K-ATP channels) in blood-brain tumor barrier (BTB). Using a rat brain glioma model, we found that DEX could significantly increase the expression of KATP channels protein at tumor sites. And bradykinin -induced increase of KATP channels protein was further enhanced after DEX pretreatment for 3 consecutive days via Western blots and immunohistochemistry methods. In addition, DEX pretreatment enhanced bradykinin-mediated increase of the density of I-KATP in the cultured rat C6 glioma cells using the patch-clamp technique in a whole-cell configuration. DEX significantly decreased the BTB permeability, but it did not reduce bradykinin-mediated BTB permeability increase, which were significantly attenuated by the KATP channel antagonist glibenclamide. This led to the conclusion that DEX-mediated change in BTB permeability is, at least partly, due to accelerated formation of KATP channel, an important target in the biochemical regulation of this process. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:1 / 8
页数:8
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