Electromagnetic pulse activated brain microglia via the p38 MAPK pathway

• Published in: Neurotoxicology (Park Forest South) 2016-01, Vol.52, p.144-149
• Main Authors: Yang, Long-Long, Zhou, Yan, Tian, Wei-Dong, Li, Hai-Juan, Kang-Chu-Li, Miao, Xia, An, Guang-Zhou, Wang, Xiao-Wu, Guo, Guo-Zhen, Ding, Gui-Rong
• Format: Article
• Language: English
• Subjects: Animals; Brain; Cerebral Cortex - cytology; Electromagnetic Fields - adverse effects; Electromagnetic pulse; Imidazoles - pharmacology; Interleukin-10 - metabolism; Interleukin-1beta - metabolism; Male; MAP Kinase Signaling System - drug effects; MAPK pathway; Microglia; Microglia - drug effects; Microglia - metabolism; Nitric Oxide - metabolism; p38 Mitogen-Activated Protein Kinases - metabolism; Primary Cell Culture; Pyridines - pharmacology; Rats; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 0161-813X; 1872-9711
• DOI: 10.1016/j.neuro.2015.12.008

•EMP exposure could activate microglia and affect its secretion function.•p38 pathway was involved. 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