Abstract
Inflammatory bowel disease (IBD), consisting of ulcerative colitis (UC) and Crohn's disease (CD), is a chronic relapsing and life-threatening inflammatory disorder that mainly affect the intestinal tract. The mainstream therapies for moderate to severe IBD lie in the use of immunosuppressive agents. However, it encountered the problem of drug tolerance and significant adverse events. Therefore, identifying novel signal pathways involved in IBD is necessary to satisfy the unmet treatment needs of IBD patients. There existed some hints between iron and IBD, and was reported that ferroptosis induced in UC. However, as another important subtype of IBD, whether ferroptosis also occurred in CD remains unclear. In this study, we found that the dysregulation of iron, lipid peroxidation and redox homeostasis were involved in CD; the administration of ferroptosis inhibitor Ferrostatin-1 could alleviate pathological phenotypes of TNBS induced CD-like colitis in mice. Our results provide a new hopeful therapeutic strategy in treating CD, especially for those who suffered from the tolerance of existing immunosuppressive agent drugs.