| Backgroud and Objective:Inflammatory bowl disease, such as ulcerative colitis and crohn's disease, is a intestinal disease which can seriously involve all the gastrointestinal tract. The canceration rate and case fatality of IBD are high. Because it has not been fully understood, it is difficult to cure it. Patients suffered a lot from it. A new study indicated that regulatory T cell is a CD4+CD25+ T cell population that comprises 5-10% of the total peripheral CD4+ T cells in a normal adult mice and expresses surface CD25 before activation. In certain strains of mice, elimination of this CD4+CD25+ T cell population by early thymectomy results in various autoimmune diseases, which, in turn, are preventable by its restoration by adaptive transfer. Similarly, transfer of CD25+-depleted splenocytes into nude mice results in various autoimmune diseases that are prevented by cotransfer of CD4+CD25+ T cells. Resent study showed that the CD4+CD25+ T cell play a central role in the body immuno system, thus in UC. In this study, we try to build a ulcerative colitis(UC) model induced by dinitrochlorobenzene (DNCB)-acetic acid(AA) in mice,to research the pathogenesis and to find the effective medicine of Traditional Chinese Medicine for UC. These mouse with UC will be cured experimentally, in which we find the mechanism of CD4+CD25+ T cell which can give reference to the clinical treat.MethodsAdult KM mouse were randomly divided into four groups: normal control group, experimental colitis model group, salazosulfapyridine (SASP) and CLYSTER No.1(CN1) therapeutic groups. Proportions of CD3+,CD4+ T cell,CD4+CD29+ T cell in mesenteric lymph node (MLN) and peripheral blood (PB) of each group were estimated by flow cytometry; and histological changes were evaluated by H.E. staining and histological score of intestine to check the availability and utility of the model. Experimental treatments were made a week later building the model. Observe the clinical symptom; Proportions of CD3+,CD4+ T cell,CD4+CD25+ T cell in mesenteric lymph node and peripheral blood of each group were estimated by flow cytometry; and histological changes were evaluated by H.E staining and histological score of intestine. Immunohistochemistry stain was made to test the IL-1βand iNOS; Foxp3 mRNA was tested by RT-PCR.Results:The model of experimental colitis in mouse was successfully established. Compared with normal control group, the histological score was markedly higher and the length of colon became shorter in model control group of experimental colitis. Identically in this group, the proportion of CD3+,CD4+ T cells were markedly decreased (P<0.05) and the proportion of CD4+CD29+ T cell was significantly increased (P<0.01) than the normal control group. After two weeks'treated with SASP and CN1, the histological score was reduced, the length of colon recovered almost to normal level and was accompanied by increase of the proportion of CD3+,CD4+ T cells compared with the experimental group. Compared with normal control group, the proportion of CD4+CD25+ Tregs was markedly decreased in PB and MLN of model control group of experimental colitis. But it was significantly increased in therapeutic groups of SASP and CN1, and their CD4+CD25+ Tregs in PB and MLN were much more than the model control group at the end of one or two weeks after treating with SASP and CN1. Foxp3 mRNA was not detected in model group, however in the treatment group, we detected a definite band of Foxp3 mRNA. We detected much more IL-1β+ and iNOS+ cells in model group than in the treatment group.Conclusions:The effect was satisfying for the UC mice treated with CN1 and it may serve as a tool for investigation of the pathogenesis and therapeutical effect for UC. CD4+CD25+ Tregs with strong immune suppression could play a central role in the initiation and development of mouse experiment colitis, and the CLYSTER No.1 might exert its therapeutic effects on UC by the refulation of number and function of CD4+CD25+ Tregs. Maybe it has something with the NF-?B signal iter.
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