Insights from advances in research of chemically induced experimental models of human inflammatory bowel disease  

作　　者：Mayumi Kawada Atsuko Arihiro Emiko Mizoguchi 

机构地区：[1]Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, United States

出　　处：《World Journal of Gastroenterology》2007年第42期5581-5593,共13页世界胃肠病学杂志（英文版）

基　　金：National Institute of Health grants,No. DK64289,DK74454,and DK43351),IBD grants from the Eli and Edythe Broad Medical Foundation

摘　　要：Inflammatory bowel disease(IBD),the most important being Crohn's disease and ulcerative colitis,results from chronic dysregulation of the mucosal immune system in the gastrointestinal tract.Although the pathogenesis of IBD remains unclear,it is widely accepted that genetic,environmental,and immunological factors are involved.Recent studies suggest that intestinal epithelial defenses are important to prevent inflammation by protecting against microbial pathogens and oxidative stresses.To investigate the etiology of IBD,animal models of experimental colitis have been developed and are frequently used to evaluate new anti-inflammatory treatments for IBD.Several models of experimental colitis that demonstrate various pathophysiological aspects of the human disease have been described.In this manuscript,we review the characteristic features of IBD through a discussion of the various chemically induced experimental models of colitis(e.g.dextran sodium sulfate-,2,4,6-trinitrobenzene sulfonic acid-,oxazolone-,acetic acid-,and indomethacin-induced models).We also summarize some regulatory and pathogenic factors demonstrated by these models that can,hopefully,be exploited to develop future therapeutic strategies against IBD.Inflammatory bowel disease （IBD）, the most important being Crohn＇s disease and ulcerative colitis, results from chronic dysregulation of the mucosal immune system in the gastrointestinal tract. Although the pathogenesis of IBD remains unclear, it is widely accepted that genetic, environmental, and immunological factors are involved. Recent studies suggest that intestinal epithelial defenses are important to prevent inflammation by protecting against microbial pathogens and oxidative stresses. To investigate the etiology of IBD, animal models of experimental colitis have been developed and are frequently used to evaluate new anti-inflammatory treatments for IBD. Several models of experimental colitis that demonstrate various pathophysiological aspects of the human disease have been described. In this manuscript, we review the characteristic features of IBD through a discussion of the various chemically induced experimental models of colitis （e.g. dextran sodium sulfate-, 2,4,6-trinitrobenzene sulfonic acid-, oxazolone-, acetic acid-, and indomethacin-induced models）. We also summarize some regulatory and pathogenic factors demonstrated by these models that can, hopefully, be exploited to develop future therapeutic strategies against IBD.

关 键 词：Inflammatory bowel disease Experimental colitis Dextran sodium sulfate Trinitrobenzene sulfonicacid OXAZOLONE PATHOGENESIS 

分 类 号：R574[医药卫生—消化系统]