当前位置: X-MOL 学术Neurotoxicology › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Electromagnetic pulse activated brain microglia via the p38 MAPK pathway.
NeuroToxicology ( IF 3.4 ) Pub Date : 2015-12-22 , DOI: 10.1016/j.neuro.2015.12.008
Long-Long Yang 1 , Yan Zhou 2 , Wei-Dong Tian 3 , Hai-Juan Li 4 , Kang-Chu-Li 2 , Xia Miao 2 , Guang-Zhou An 2 , Xiao-Wu Wang 4 , Guo-Zhen Guo 4 , Gui-Rong Ding 2
Affiliation  

Previously, we found that electromagnetic pulses (EMP) induced an increase in blood brain barrier permeability and the leakage of albumin from blood into brain tissue. Albumin is known to activate microglia cells. Thus, we hypothesised that microglia activation could occur in the brain after EMP exposure. To test this hypothesis, the morphology and secretory function of microglia cells, including the expression of OX-42 (a marker of microglia activation), and levels of TNF-α, IL-10, IL-1β, and NO were determined in the rat cerebral cortex after EMP exposure. In addition, to examine the signalling pathway of EMP-induced microglia activation, protein and phosphorylated protein levels of p38, JNK and ERK were determined. It was found that the expression of OX-42increased significantly at 1, 6 and 12h (p<0.05) and recovered to the sham group level at 24h after EMP exposure. Levels of NO, TNF-α and IL-10 also changed significantly in vivo and in vitro after EMP exposure. The protein level of p38 and phosphorylated p38 increased significantly after EMP exposure (p<0.05) and recovered to sham levels at 12 and 24h, respectively. Protein and phosphorylated protein levels of ERK and JNK did not change. SB203580 (p38 inhibitor) partly prevented the change in NO, IL-10, IL-1β, TNF-α levels induced by EMP exposure. Taken together, these results suggested that EMP exposure (200kV/m, 200 pulses) could activate microglia in rat brain and affect its secretory function both in vivo and in vitro, and the p38 pathway is involved in this process.

中文翻译:

电磁脉冲通过p38 MAPK途径激活脑小胶质细胞。

以前,我们发现电磁脉冲(EMP)引起血脑屏障通透性的增加以及白蛋白从血液泄漏到脑组织中。已知白蛋白可激活小胶质细胞。因此,我们假设暴露于EMP后小胶质细胞活化可能发生在大脑中。为了验证这一假设,测定了小胶质细胞的形态和分泌功能,包括OX-42(小胶质细胞激活的标记)的表达以及TNF-α,IL-10,IL-1β和NO的水平。 EMP暴露后的大鼠大脑皮层。此外,为检查EMP诱导的小胶质细胞活化的信号传导途径,测定了p38,JNK和ERK的蛋白和磷酸化蛋白水平。发现OX-42的表达在1、6和12h显着增加(p <0。05),在暴露于EMP后24小时恢复到假组水平。EMP暴露后体内和体外的NO,TNF-α和IL-10水平也发生了显着变化。EMP暴露后,p38和磷酸化的p38的蛋白质水平显着增加(p <0.05),并分别在12h和24h恢复到假水平。ERK和JNK的蛋白质和磷酸化蛋白质水平没有变化。SB203580(p38抑制剂)部分阻止了EMP暴露引起的NO,IL-10,IL-1β,TNF-α水平的变化。综上所述,这些结果表明EMP暴露(200kV / m,200个脉冲)可以激活大鼠脑内的小胶质细胞,并在体内和体外影响其分泌功能,而p38途径参与了这一过程。EMP暴露后,TNF-α和IL-10在体内和体外也发生了显着变化。暴露于EMP后,p38和磷酸化p38的蛋白质水平显着增加(p <0.05),并分别在12h和24h恢复到假水平。ERK和JNK的蛋白质和磷酸化蛋白质水平没有变化。SB203580(p38抑制剂)部分阻止了EMP暴露引起的NO,IL-10,IL-1β,TNF-α水平的变化。综上所述,这些结果表明EMP暴露(200kV / m,200个脉冲)可以激活大鼠脑内的小胶质细胞,并在体内和体外影响其分泌功能,而p38途径参与了这一过程。EMP暴露后,TNF-α和IL-10在体内和体外也发生了显着变化。EMP暴露后,p38和磷酸化的p38的蛋白质水平显着增加(p <0.05),并分别在12h和24h恢复到假水平。ERK和JNK的蛋白质和磷酸化蛋白质水平没有变化。SB203580(p38抑制剂)部分阻止了EMP暴露引起的NO,IL-10,IL-1β,TNF-α水平的变化。综上所述,这些结果表明EMP暴露(200kV / m,200个脉冲)可以激活大鼠脑内的小胶质细胞,并在体内和体外影响其分泌功能,而p38途径参与了这一过程。ERK和JNK的蛋白质和磷酸化蛋白质水平没有变化。SB203580(p38抑制剂)部分阻止了EMP暴露引起的NO,IL-10,IL-1β,TNF-α水平的变化。综上所述,这些结果表明EMP暴露(200kV / m,200个脉冲)可以激活大鼠脑内的小胶质细胞,并在体内和体外影响其分泌功能,而p38途径参与了这一过程。ERK和JNK的蛋白质和磷酸化蛋白质水平没有变化。SB203580(p38抑制剂)部分阻止了EMP暴露引起的NO,IL-10,IL-1β,TNF-α水平的变化。综上所述,这些结果表明EMP暴露(200kV / m,200个脉冲)可以激活大鼠脑内的小胶质细胞,并在体内和体外影响其分泌功能,而p38途径参与了这一过程。
更新日期:2015-12-10
down
wechat
bug