Objective  In addition to being the organ responsible for digestion and absorption of nutrients, the intestine serves a barrier function that is a critical component of the innate immune system.Only a single layer of epithelial cells separates the luminal contents from effector immune cells in the lamina propria and the internal milieu of the body. Complete intestinal barrier is comprised of 1.The mechanical barrier is comprised of continual epithelial of gut mucosal;2.Cellular and humoral immunity provided by lymphoid tissue of intestinal tract;3.Normal and massive commensal intestinal bacterial clusters,preventing the over proliferating and permanent planting in gut mucosal of pathogenic microorganism.  The mechanical barrier is comprised of mucus,microvilli,epithelial cells and junctions among them and other particular constructions,which is the structural foundation of intestinal mucosal barrier.Not only the morphous change of epithelial cells but also the wideness of junction gap and the increasing of opened cell-cell junctions could affect the function of intestinal epithelial barrier and increase the permeability.The disruption of barrier integrity has been implicated in the pathogenesis of a wide variety of gastrointestinal and systemic disorders such as inflammatory bowel disease,liver failure,acute severe pancreases and multiple organ system failure.In addition to these,many acute and chronic gastrointestinal and systemic disorders in paediatrics such as sepsis,eczema,food allergies,celiac enteropathy,type 1 diabetes, asthma,and so on were also implicated in,Hense studying the mechanisms of high permeability and to explore the effectual treatment become the goal of this experiment.  The increase of intestinal epithelial barrier permeability implicated in several factors,including initiatal causative agent as infection or ischemia and secondum inflammatory mediator.In recent years,the roles of platelet activating factor(PAF)to impairment of gastrointestinal mucosa has been paid increasing attention.PAF can be produced by intestinal epithelial cells and constitutively present in normal small intestinal tissue regulating the mucosal permeability.A large body of evidence suggests that PAF is involved in the pathogenesis of intestinal injury in various diseases.Moreover,PAF at doses insufficient to cause bowel necrosis triggers the expression of cytokines,and activates transcription factors in the intestine.So PAF is regarded as central amplify mediator and key factor of increasing of intestinal epithelial barrier permeability.  The mechanisms of PAF-related epithelial breakdown are unclear,but regulation of paracellular pathways,especially via rearranging cytoskeleton F-actin and changing interepithelial tight junction(TJ)proteins such as Occludin,Claudin-1,ZO-1 is likelyto play a significant role.Therefore,we detect the effect of PAF on intestinal epithelial F-actin and interepithelial tight junction via in vitro intestinal epithelia barrier models established with Caco-2 cells to study the mechanisms involved in disruption of intestinal epithelium mechanical barrier induced by PAF.  Intestinal trefoil factor(ITF)is a member of trefoil peptide family,which is important in maintenance and reparation of the intestinal mucosal barrier.It can not only stimulate cell migrating and proliferating,promote epithelial cell reparation,but also interact with the mucus,stabilize the mucus gel by perhaps interacting with intestinal mucin and increasing the viscosity.So it is important in the self-protection mechanism of intestine.Many researches in vivo also demonstrated ITF was important in the maintenance of intestinal epithelium barrier integrity and in the rescovery of mucosal normal permeability.Recent in vitro experiment find ITF can regulate the expression of TJ proteins of Claudin-1 and Claudin-2,then to affect TEER.But whether PAF can affect the expression of ITF? Administer of rITF can protect the intestinal mucosal barrier? What is the mechanisms? To answer these questions and to provide theory base for clinical application of rITF were the basic consideration of this study.  Materials and methods  1.Cell cultures   Caco-2 cells were grown in a culture medium composed of RPMI 1640 with 4.5 mg/ml glucose,50 U/ml penicillin,50 U/ml streptomycin,and 15