Exposure to electromagnetic field attenuates oxygen-glucose deprivation-induced microglial cell death by reducing intracellular Ca(2+) and ROS
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Published on: October 21, 2017
Cao Nguyen Duong1, Jae Young Kim1
1a Department of Life Science , Gachon University , Seongnam , Kyeonggi-Do , Korea.
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 4 h under OGD with or without exposure to EMF with different combinations of frequencies and intensities (10, 50, or 100 Hz/1 mT and 50 Hz/0.01, 0.1, or 1 mT). 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 Ca(2+) and ROS levels. Among different combinations of EMF frequencies and intensities, 50 Hz/1 mT EMF was the most potent to attenuate OGD-induced cell death and intracellular Ca(2+) and ROS levels. A significant but less potent protective effect was also found at 10 Hz/1 mT, 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 50 Hz/1 mT EMF protects human microglial cells from OGD-induced cell death by interfering with OGD-induced elevation of intracellular Ca(2+) 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.
Insights
Electromagnetic field (EMF) exposure, specifically at 50 Hz/1 mT, protected human microglial cells from oxygen-glucose deprivation (OGD)-induced death. This EMF treatment reduced cell death by lowering reactive oxygen species (ROS) and intracellular calcium levels.
Area of Science:
- Neuroscience
- Biophysics
- Cell Biology
Background:
- Microglial cells are crucial for brain immune responses.
- Ischemic conditions, like oxygen-glucose deprivation (OGD), trigger cell death in microglial cells.
- Reactive oxygen species (ROS) and intracellular calcium (Ca2+) are key mediators of ischemic cell death.
Purpose of the Study:
- To investigate the protective effects of electromagnetic field (EMF) exposure against OGD-induced cell death in the human microglial cell line HMO6.
- To determine the optimal EMF frequency and intensity for neuroprotection.
Main Methods:
- HMO6 cells were subjected to OGD with varying EMF exposures (frequencies: 10, 50, 100 Hz; intensities: 0.01, 0.1, 1 mT).
- Cell survival, intracellular Ca2+, and ROS levels were quantified.
- Inhibitors of xanthine oxidase, NADPH oxidase, and mitochondrial complex II were used to identify ROS pathways.
Main Results:
- OGD significantly increased HMO6 cell death, intracellular Ca2+, and ROS levels.
- EMF exposure at 50 Hz/1 mT demonstrated the most potent protective effect, significantly reducing cell death and associated molecular markers.
- A protective effect was also observed at 10 Hz/1 mT, but less pronounced. Xanthine oxidase inhibition reversed OGD-induced ROS and cell death.
Conclusions:
- 50 Hz/1 mT EMF protects human microglial cells against OGD-induced death by modulating intracellular Ca2+ and ROS levels.
- Xanthine oxidase plays a significant role in OGD-induced microglial cell death.
- EMF radiation presents a potential non-invasive therapeutic strategy for hypoxic-ischemic brain injury.
