Effect Of Vitamin A On Tight Junction Protein Expression And Inhibition Of Intestinal Inflammation

Objectives: Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown.Most diseases is related with the gut mucosal barrier function in the clinic.Intestinal barrier refers to the function of the intestinal epithelium to separate the intestinal cavity and prevent the invasion of pathogenic antigens.Tight junctions constitute an important part of the intestinal barrier,which form a barrier to the connection between the intestinal epithelial cells to maintain the tissue homeostasis.The integrity and permeability of intestinal epithelial will affect the normal function of the intestinal tract.Tight junctions between epithelial cells form a barrier that maintains tissue homeostasis.The intestinal epithelial barrier can become leaky as a result of genetic predisposition intestinal pathogens and hyperglycemia resulting in IBD,autoimmunity,and systemic inflammation.This thesis will uncover effect of vitamin A on tight junction protein expression and its inhibition of intestinal inflammation.Methods: TEER detected that LPS induced significantly the decrease of TEER In contrast,0.1 μ mol/L Vitamin A alone dramatically increased TEER,indicating that Vitamin A reduced intestinal epithelium permeability.Co-treatment of Vitamin A and LPS demonstrated that Vitamin A repaired LPS-induced intestinal tight junction permeability in IPEC-J2 cells.Different concentrations of Vitamin A(0-20 μmol/L)detected up-regulation of tight junction Zo-1,Occludin,Claudin-1 protein and m RNA by WB and RT-PCR.Animal experiments in weaned piglets showed that Vitamin A up-regulated the expression of tightly linked structural proteins Zo-1,Occludin,Claudin-1 protein and m RNA in intestinal tissues,and the most significant effect on duodenum.Conclusion: Vitamin A enhance the expression of Zo-1 and alleviate LPS-induced intestinal inflammation;Vitamin A have a protective effect on gut-intestinal barrier structure proteins.