In the present study, we demonstrate that sodium butyrate repressed IFN-γ-induced expression of iNOS and TNF-α, but had little effect on LPS-induced expression in BV2 murine microglial cells. Sodium butyrate significantly inhibited NF-κB binding and NF-κB-mediated transcription induced by IFN-γ, suggesting that the anti-inflammatory effect of sodium butyrate is mediated via specific inhibition of the NF-κB pathway. IFN-γ is a major stimulator of innate and adaptive immune response. Thus, the specific down-regulation of IFN-γ-induced microglial activation by sodium butyrate may provide potential therapeutic strategies for a variety of inflammatory diseases in the central nervous system.
Bibliographical noteFunding Information:
This work was supported by a grant to H.S. Kim (03-PJ1-PG3-21300-0047) from the Korea Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea.
- Sodium butyrate
ASJC Scopus subject areas
- Immunology and Allergy
- Clinical Neurology