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Nanog is an essential transcription factor maintaining the self-renewaland pluripotency of embryonic stem cells, which binds to nuclear factor-κB (NF-κB)proteins, inhibits their transcriptional activity and represses their pro-differentiationactivity. The persistent and excessive activation of microglial cells, as primaryimmune cells in the central nervous system is associated with various nerve systemdiseases, such as neuropathic pain, ischemia, infection, as well as neurodegenerativediseases. However, the effects of Nanog on the activation of microglial cellshave yet to be elucidated. In this study, we investigated whether Nanog inhibitsthe production of pro-inflammatory factors in lipopolysaccharide (LPS)-stimulatedmicroglial cells. Nanog was shown to down-regulate the mRNA and protein levelsof 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 reducedby Nanog, which was measured using luciferase assay. The results suggest thatNanog reduces the production of pro-inflammatory cytokines and attenuates inflammatoryresponses in LPS-stimulated microglial cells by blocking the transcriptional activityof NF-κB. Thus, Nanog may be a potentially useful anti-inflammatory therapy forthe treatment of various nervous system diseases.

molecular medicine reports

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