Background:

Sodium butyrate is a short chain fatty acid that has effects at the molecular, cellular, and tissue level. It has long been known as an inhibitor of histone deacetylases (HDACs).[1],[2] In cells, this alters the expression of a select group of genes containing butyrate response elements and may also involve Sp1/Sp3 binding sites.[3] Sodium butyrate also induces growth arrest, differentiation and apoptosis in cancer cells, primarily through its effects on HDAC activity.[4] In addition, it suppresses inflammation, in part by reducing the expression of pro-inflammatory cytokines, including interferon-γ, interleukin (IL)-6, and IL-1β.[5]
Reference:
[1]. Boffa, L.C., Vidali, G., Mann, R.S., et al. Suppression of histone deacetylation in vivo and in vitro by sodium butyrate. The Journal of Biological Chemisty 253(10), 3364-3366 (1978).
[2]. Sealy, L., and Chalkley, R. The effect of sodium butyrate on histone modification. Cell 14, 115-121 (1978).
[3]. Davie, J.R. Inhibition of histone deacetylase activity by butyrate. Journal of Nutrition 133, 2485-2493 (2003).
[4]. Monneret, C. Inhibition of histone deacetylase activity by butyrate. European Journal of Medicinal Chemistry 40, 1-13 (2005).
[5]. Joseph, J., Mudduluru, G., Antony, S., et al. Expression profiling of sodium butyrate (NaB)-treated cells: identification of regulation of genes related to cytokine signaling and cancer metastasis by NaB. Oncogene 23, 6304-6315 (2004).