Nanog inhibits lipopolysaccharide-induced expression of pro-inflammatory cytokines by blocking NF-κB transcriptional activity in rat primary microglial cells

Abstract

Nanog is an essential transcription factor maintaining the self-renewal and pluripotency of embryonic stem cells, which binds to nuclear factor-κB (NF-κB) proteins, inhibits their transcriptional activity and represses their pro-differentiation activity. The persistent and excessive activation of microglial cells, as primary immune cells in the central nervous system is associated with various nerve system diseases, such as neuropathic pain, ischemia, infection, as well as neurodegenerative diseases. However, the effects of Nanog on the activation of microglial cells have yet to be elucidated. In this study, we investigated whether Nanog inhibits the production of pro-inflammatory factors in lipopolysaccharide (LPS)-stimulated microglial cells. Nanog was shown to down-regulate the mRNA and protein levels of IL-1β, TNF-α and IL-6 in LPS-stimulated rat primary microglial cells. Furthermore, we also found that the transcriptional activity of NF-κB was dramatically reduced by Nanog, which was measured using luciferase assay. The results suggest that Nanog reduces the production of pro-inflammatory cytokines and attenuates inflammatory responses in LPS-stimulated microglial cells by blocking the transcriptional activity of NF-κB. Thus, Nanog may be a potentially useful anti-inflammatory therapy for the treatment of various nervous system diseases.