Silent information regulator-1 (SIRT-1), is a member of the class III group of histone deacetylases and is collectively called sirtuins. There have been preclinical and clinical studies indicating the downregulation and decreased activity of sirtuin 1 in various inflammatory bowel disease models. Furthermore, the downregulation of sirtuin 1 is responsible for the sustained production of proinflammatory cytokines and the generation of oxidative stress in colitis. Hyperacetylation of NF-κB and HSF-1 (heat shock factor-1) in the absence of sirtuin1 is responsible for the induction of colitis. Accordingly, exogenous administration of sirtuin1 activators has been shown to attenuate the colitis in various inflammatory bowel disease models. On the other hand, the knockdown of sirtuin 1 gene or pharmacologic inhibition of sirtuin 1 has also been shown to be protective in the colitis. The deletion of the sirtuin1 gene may be helpful in the improvement of the disease condition of colitis through the maintenance of gastrointestinal immune homeostasis. The current review highlights the dual role of sirtuin 1 in the different experimental models of IBD along with possible mechanisms.

沉默信息调节剂1（SIRT-1）是组蛋白脱乙酰基酶的III类组的成员，统称为sirtuins。临床前和临床研究表明，在各种炎症性肠病模型中，sirtuin 1的表达下调和活性降低。此外，Sirtuin 1的下调导致结肠炎中持续产生促炎性细胞因子和氧化应激。在缺少sirtuin1的情况下，NF-κB和HSF-1（热休克因子-1）的过度乙酰化是导致结肠炎的原因。因此，在多种炎症性肠病模型中，外源给予sirtuin1激活剂可减轻结肠炎。另一方面，sirtuin 1基因的敲低或sirtuin 1的药理抑制作用也已显示出对结肠炎具有保护作用。sirtuin1基因的缺失可能通过维持胃肠道免疫稳态而有助于改善结肠炎的疾病状况。当前的评论强调了sirtuin 1在IBD的不同实验模型中的双重作用以及可能的机制。