The role of protein kinase C in the opening of blood-brain barrier induced by electromagnetic pulse
The role of protein kinase C in the opening of blood-brain barrier induced by electromagnetic pulse
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蛋白激酶C在电磁脉冲诱导血脑屏障开放中的作用
DOI：
10.1016/j.tox.2010.04.013
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发表时间：
2010-06-29
期刊：
影响因子：
4.5
通讯作者：
Guo, Guo-Zhen
中科院分区：
文献类型：
--
作者：
Qiu, Lian-Bo;Ding, Gui-Rong;Guo, Guo-Zhen
本研究旨在探讨蛋白激酶C信号在电磁脉冲（EMP）诱导的大鼠血脑屏障（BBB）通透性改变中的作用。在200 kV/m、1 Hz重复频率、200个脉冲的电磁脉冲下，通过Western blot检测大鼠大脑皮层微血管中总PKC和两种PKC亚型（PKC-α和PKC-β II）的蛋白水平。结果发现，与假暴露组相比，EMP暴露后0.5h和1h，大脑皮质微血管中PKC和PKC-β II（而非PKC-α）蛋白水平显著升高，3 h后恢复正常。一种特异性的PKC拮抗剂（H7）几乎可以阻断EMP引起的血脑屏障通透性的改变。EMP诱导的BBB紧密连接蛋白ZO-1转位也受到抑制。提示PKC信号通路参与了EMP诱导的大鼠血脑屏障通透性改变和ZO-1转位。(C)2010爱思唯尔爱尔兰有限公司版权所有。
The aim of this study was to determine the role of protein kinase C signaling in electromagnetic pulse (EMP)-induced blood brain barrier (BBB) permeability change in rats. The protein level of total PKC and two PKC isoforms (PKC-alpha, and PKC-beta II) were determined in brain cerebral cortex microvessels by Western blot after exposing rats to EMP at 200 kV/m for 200 pulses with 1 Hz repetition rate. It was found that the protein level of PKC and PKC-beta II (but not PKC-alpha) in cerebral cortex microvessels increased significantly at 0.5 h and 1 h after EMP exposure compared with sham-exposed animals and then recovered at 3 h. A specific PKC antagonist (H7) almost blocked EMP-induced BBB permeability change. EMP-induced BBB tight junction protein ZO-1 translocation was also inhibited. Our data indicated that PKC signaling was involved in EMP-induced BBB permeability change and ZO-1 translocation in rat. (C) 2010 Elsevier Ireland Ltd. All rights reserved.