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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >The role of protein kinase C in the opening of blood-brain barrier induced by electromagnetic pulse.
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The role of protein kinase C in the opening of blood-brain barrier induced by electromagnetic pulse.

机译:蛋白激酶C在电磁脉冲诱导的血脑屏障打开中的作用。

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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 200kV/m for 200 pulses with 1Hz repetition rate. It was found that the protein level of PKC and PKC-betaII (but not PKC-alpha) in cerebral cortex microvessels increased significantly at 0.5h and 1h after EMP exposure compared with sham-exposed animals and then recovered at 3h. 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.
机译:这项研究的目的是确定蛋白激酶C信号在大鼠电磁脉冲(EMP)诱导的血脑屏障(BBB)通透性变化中的作用。在大鼠以200kV / m的EMP频率以200 Hz / m的频率以1Hz的重复频率暴露于EMP后,通过Western blot测定了大脑皮层微血管中总PKC和两种PKC亚型(PKC-α和PKC-βII)的蛋白水平。结果发现,与假手术动物相比,EMP暴露后0.5h和1h,大脑皮层微血管中PKC和PKC-βII(而不是PKC-α)的蛋白质水平显着增加,然后在3h时恢复。特定的PKC拮抗剂(H7)几乎阻止了EMP诱导的BBB通透性变化。 EMP诱导的BBB紧密连接蛋白ZO-1易位也受到抑制。我们的数据表明,PKC信号传导参与了EMP诱导的大鼠BBB通透性变化和ZO-1易位。

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