New class of anti-inflammatory agents for colonic epithelial cells Dan Gordon  Gastroenterology  Volume 117, Issue 5, (November 1999) DOI: 10.1016/S0016-5085(99)70382-3 Copyright © 1999 Terms and Conditions

NF-κB transduces signals from many types of proinflammatory agents, leading to production of cytokines that promote the inflammatory response. Glucocorticoids prevent the first step of NF-κB activation, dissociation of an inhibitor known as IKB and translocation of activated NF-κB to the nucleus. The nuclear receptor known as PPAR-γ, when activated, prevents transcriptional activation of proinflammatory genes by NF-κB. Drugs that can activate PPAR-γ, including thiazolidinedione antidiabetic drugs and certain prostaglandins, thus can exert anti-inflammatory effects. This system appears to be very active in colonic epithelial cells and may serve as an alternate target for treatment of inflammatory bowel disease. Gastroenterology 1999 117, DOI: (10.1016/S0016-5085(99)70382-3) Copyright © 1999 Terms and Conditions