关键词: 马齿苋多糖, 溃疡性结肠炎, IL-6/STAT3, NF-κB、大鼠

Abstract: Objective: 2minus 2-trinitrobenzene sulfonic acid (TNBS) copy ulcerative colitis model of rats, to explore purslane polysaccharide on ulcerative colitis rats colon organization IL6/STAT3 and the influence of the NF-kappa B, clear IL-6/STAT3 signaling pathway and the relationship of chronic inflammatory bowel disease, looking for new targets for the treatment of chronic ulcerative colitis.Methods: Fourty rats were randomly divided into control group, model group, mesalazine group, and purslane group (n=10). The colonic contents were weighed and weighed again after drying, and the colonic tissues were biopsies. The contents of serum interleukin-6 (IL-6), interleukin 1 β (IL-1 β), tumor necrosis factor α (TNF-α), nuclear transcription factor kappa B (NF-kappa B) were detected by ELISA kit. Immunohistochemical staining was used to determine the colonic MPO (myeloperoxidase). RT-PCR method was used to detect signal transduction and transcriptional activator 3 (STAT3), IL-6 mRNA.Results: Compared with model group and mesalazine group, defecation status of rats in purslane group were markedly improved, intestinal mucosa edema reduced, the serum IL-6, intestinal tissue MPO, the NF-kappa B and serum sIL-6Rα, gp130 content were decreased (P<0.01). Compared with the model group, the expression levels of STAT3 and IL-6 mRNA in the purslane group were significantly reduced (P<0.01). There was no significant difference of testing indicator mentioned above between control group and purslane group (P>0.05).Conclusion: By lowering the serum IL-6, sIL-6Rα and gp130 in rats, the purslane polysaccharides reduced the levels of MPO and NF-kappa B in the intestinal tissues, and further reduced the inflammatory response caused by the formation of sIL-6R alpha and IL-6. By using IL-6/STAT3 signaling pathway, the mRNA expression levels of STAT3 and IL-6 of rats intestinal tissues were down-regulated to inhibit the occurrence of inflammation.

Key words: Purslane polysaccharide, inflammatory bowel disease, IL-6/STAT3 signaling pathway, rat