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Exposure to electromagnetic field attenuates oxygen-glucose deprivation-induced microglial cell death by reducing intracellular Ca2+ and ROS

Authors
Cao Nguyen DuongKim, Jae Young
Issue Date
2-Apr-2016
Publisher
TAYLOR & FRANCIS LTD
Keywords
Electromagnetic field; microglia; HMO6; ischemic injury; Ca2+; reactive oxygen species
Citation
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY, v.92, no.4, pp.195 - 201
Journal Title
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY
Volume
92
Number
4
Start Page
195
End Page
201
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/8375
DOI
10.3109/09553002.2016.1136851
ISSN
0955-3002
Abstract
Purpose The aim of this research was to demonstrate the protective effects of electromagnetic field (EMF) exposure on the human microglial cell line, HMO6, against ischemic cell death induced by in vitro oxygen-glucose deprivation (OGD).Materials and methods HMO6 cells were cultured for 4h under OGD with or without exposure to EMF with different combinations of frequencies and intensities (10, 50, or 100Hz/1mT and 50Hz/0.01, 0.1, or 1mT). Cell survival, intracellular calcium and reactive oxygen species (ROS) levels were measured.Results OGD caused significant HMO6 cell death as well as elevation of intracellular Ca2+ and ROS levels. Among different combinations of EMF frequencies and intensities, 50Hz/1mT EMF was the most potent to attenuate OGD-induced cell death and intracellular Ca2+ and ROS levels. A significant but less potent protective effect was also found at 10Hz/1mT, whereas no protective effect was found at other combinations of EMF. A xanthine oxidase inhibitor reversed OGD-induced ROS production and cell death, while NADPH oxidase and mitochondrial respiration chain complex II inhibitors did not affect cell death.Conclusions 50Hz/1mT EMF protects human microglial cells from OGD-induced cell death by interfering with OGD-induced elevation of intracellular Ca2+ and ROS levels, and xanthine oxidase is one of the main mediators involved in OGD-induced HMO6 cell death. Non-invasive treatment of EMF radiation may be clinically useful to attenuate hypoxic-ischemic brain injury.
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