Abstract
Extremely low frequency electromagnetic fields (ELF-EMFs) have been known to modulate inflammatory responses by targeting signal transduction pathways and influencing cellular redox balance through the generation of oxidants and antioxidants. Here, we studied the molecular mechanism underlying the anti-oxidative effect of ELF-EMF in THP-1 cells, particularly with respect to antioxidant enzymes, such as heme oxygenase-1 (HO-1), regulated transcriptionally through nuclear factor E2-related factor 2 (Nrf2) activation. Cells treated with lipopolysaccharides (LPS) were exposed to a 50 Hz, 1 mT extremely low frequency electromagnetic fields for 1 h, 6 h and, 24 h. Our results indicate that ELF-EMF induced HO-1 mRNA and protein expression in LPS-treated THP-1 cells, with peak expression at 6 h, accompanied with a concomitant migration to the nucleus of a truncated HO-1 protein form. The immunostaining analysis further verified a nuclear enrichment of HO-1. Moreover, ELF-EMF inhibited the protein expressions of the sirtuin1 (SIRT1) and nuclear factor kappa B (NF-kB) pathways, confirming their anti-inflammatory/antioxidative role. Pretreatment with LY294002 (Akt inhibitor) and PD980559 (ERK inhibitor) inhibited LPS-induced Nrf2 nuclear translocation and HO-1 protein expression in ELF-EMF-exposed cells. Taken together, our results suggest that short ELF-EMF exposure exerts a protective role in THP-1 cells treated with an inflammatory/oxidative insult such as LPS, via the regulation of Nrf-2/HO-1 and SIRT1 /NF-kB pathways associated with intracellular glutathione (GSH) accumulation.
Highlights
The immune response is a signal-mediated reaction to tissue invasion by pathogens, toxins, physical injury, or stress
Our results suggest that short extremely low frequency electromagnetic fields (ELF-electromagnetic fields (EMFs)) exposure exerts a protective role in THP-1 cells treated with an inflammatory/oxidative insult such as LPS, via the regulation of Nrf-2/heme oxygenase-1 (HO-1) and SIRT1 /nuclear factor kappa B (NF-kB) pathways associated with intracellular glutathione (GSH) accumulation
HO-1 protein and mRNA expression were evaluated in lipopolysaccharides (LPS)-treated THP-1 cells that were either extremely low frequency (ELF)-EMF-exposed or sham-exposed for different amounts of times (1 h, 6 h, and 24 h) (Figure 1)
Summary
The immune response is a signal-mediated reaction to tissue invasion by pathogens, toxins, physical injury, or stress. It is triggered by signal transduction, which mediates changes to cell metabolism, and gene transcription, which leads cell response to environmental stimuli. In the progression of many inflammatory diseases, reactive oxygen species (ROS) may play a key role, and monocytes respond to oxidative stress with an upregulation of enzymes involved in adaptive survival response. We investigated the effect and the action mechanism of 50 Hz ELF-EMF on monocytic leukemia THP-1 cells, which are accepted as a good model of human monocytes/macrophages [13]. Interference of the inhibitor of Erk and Akt was used to study the likely mechanism of ELF-EMF on the oxidative balance in THP-1 cells
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