The molecular mechanism of dexamethasone-mediated effect on the blood-brain tumor barrier permeability in a rat brain tumor model

被引：38
作者：
Gu, Yan-ting [1 ]
Qin, Li-juan [2 ]
Qin, Xin [3 ]
Xu, Feng [1 ]
机构：
[1] Shenyang Pharmaceut Univ, Dept Physiol, Inst Life Sci & Biol Pharmacopedia, Shenyang 110016, Liaoning Prov, Peoples R China
[2] Inner Mongolia Med Coll, Coll Basic Med Sci, Dept Physiol, Hohhot 010059, Peoples R China
[3] China Med Univ, Coll Basic Med, Dept Physiol, Shenyang 110001, Liaoning Prov, Peoples R China
来源：
NEUROSCIENCE LETTERS | 2009年 / 452卷 / 02期
关键词：
Dexamethasone; Blood-tumor barrier; Calcium-activated potassium channel; Glioma; ACTIVATED POTASSIUM CHANNELS; GLUCOCORTICOIDS; RESISTANCE; INHIBITION; MODULATION; EXPRESSION; ARTERIES; GLIOMA; CELLS;
D O I：
10.1016/j.neulet.2008.12.047
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 calcium-activated potassium channels (K-Ca channels) and Occludin protein in blood-brain tumor barrier (BTB). Using a rat brain glioma model, we found that the expression Of K-Ca channels protein and Occludin protein was significantly increased in brain tumor tissue after DEX treatment for 3 days. Compared with non-DEX-treated animals, Evans Blue levels were greatly attenuated in DEX-treated animals. These effects were significantly reversed by the glucocorticoid receptor antagonist RU38486. In addition, DEX treatment enhanced the density of l(KCa), in the rat brain microvascular endothelial cells (RBMECs) in vitro BTB. All of these results strongly suggest that DEX could be involved in the regulation of both transcellular and paracellular pathway. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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收藏
页码：114 / 118
页数：5
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