NFKB1 and colitis: SIRT1 directly interacts with the RelA/p65 subunit of NF-κB, leading to deacetylation and subsequent inactivation of NF-κB.30 However, siRNA knockdown of SIRT1 augmented acetylation of RelA/p65, as well as release of IL-8, in a monocyte–macrophage cell line.29 In the dextran sodium sulfate-induced murine colitis model, resveratrol upregulated SIRT1 expression and abrogated NF-κB activation, thus attenuating intestinal inflammation.31 In addition to NF-κB, SIRT1 inhibits other transcription factors, including those that orchestrate proinflammatory responses.