Isoflurane preconditioning ameliorates electromagnetic pulse-induced neural damage by shifting microglia polarization toward anti-inflammatory phenotype via upregulation of SOCS1
| Autor: | Liying Tian, Changjun Gao, Xuqin Zhu, Jiangjing Li, Miao-Miao Lv, Xude Sun, Xiajing Zhang, Yongping Shao |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Male Chemokine Immunology Neuroprotection Cell Line Rats Sprague-Dawley 03 medical and health sciences Mice 0302 clinical medicine Electromagnetic Fields Suppressor of Cytokine Signaling 1 Protein Downregulation and upregulation In vivo medicine Immunology and Allergy Animals Neuroinflammation Pharmacology Neurons biology Microglia Isoflurane Chemistry Suppressor of cytokine signaling 1 Cell Polarity Cell biology Up-Regulation 030104 developmental biology medicine.anatomical_structure Neuroprotective Agents Phenotype 030220 oncology & carcinogenesis TLR4 biology.protein Cytokines Electromagnetic Phenomena |
| Zdroj: | International immunopharmacology. 68 |
| ISSN: | 1878-1705 |
| Popis: | With the speedy technological advances during the past few decades, human exposure to the electromagnetic field (EMF) has become increasingly common. Exposure to EMF may induce neural injuries and dysfunction of various organs, likely involving neuroinflammation and activation of microglial cells. Isoflurane preconditioning (IP) is shown to provide neuroprotection in various neurological diseases by inhibiting excessive neuroinflammatory responses. Brain samples harvested from rats exposed to electromagnetic pulse (EMP) with or without IP were subjected to qPCR, Western blot assay, and immunohistochemistry to determine the expression of pro-inflammatory/anti-inflammatory microglia markers and a variety of pro- and anti-inflammatory mediators. Suppressor of cytokine signaling 1 (SOCS1) siRNA was used in cultured N9 microglia cells to examine the roles of SOCS1 in the effect of IP. In both in vivo and in vitro experiments, EMP-exposed microglia were predominantly pro-inflammatory microglia, accompanied by increased expression of pro-inflammatory cytokines and chemokines, and activation of TLR4 pathway, leading to neuronal death. IP reversed the changes induced by EMP and switched the activated microglia to an anti-inflammatory phenotype. SOCS1 siRNA abolished the beneficial effects of IP. IP ameliorates EMP-induced neural injuries by shifting microglia polarization from pro-inflammatory to anti-inflammatory phenotype via upregulation of SOCS1. |
| Databáze: | OpenAIRE |
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