Abstract

The role of p38 mitogen-activated protein kinase in regulating the cell responses to ultralow-intensity centimeter microwaves (8.15–18.0 GHz, 1 µW/cm2, 1 h) was studied in male BalbC mice. Mice were tested for the level of protein phosphorylation in the NF-κB (p65 and IKK), JNK, and IRF3 signaling cascades expression of TLR4 and stress-inducible heat shock proteins Hsp72 and Hsp90 in splenic lymphocytes and pro- and anti-inflammatory cytokines and IL-10 in the blood serum. An inhibitor of the p38 signaling pathway (p38 inhibitor XI) was shown to reduce the sensitivity to ultralow-intensity ultrahigh-frequency electromagnetic radiation. This was evident from a decrease in radiation-induced activation of the NF-κB signaling pathway, expression of Hsp72 and Hsp90 in splenic cells, and an accumulation of proinflammatory cytokines (IL-6, IL-17, TNF-α, and IFN-γ) in the blood serum of irradiated mice pretreated with p38 inhibitor XI. However, p38 inhibitor XI did not attenuate the activation of the p38 and IRF3 signaling pathways and overexpression of TLR4 in splenic cells of irradiated mice. It was assumed that p38 mitogenactivated protein kinase is involved in regulating the nonspecific defense responses does not determine the murine sensitivity to ultralow-intensity electromagnetic waves of the centimeter range.

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