| Nervous-endocrine-immune form a complex network-neuroendocrine-immune regulation network, which controls the body's various life activities, maintain homeostasis of the body. When the homeostasis is disrupted, certain parts in the network will respond and do some change in the function, meanwhile, related link in the network show some change, leading to Certain diseases and the emergence of pathological process. Neuroendocrine and immune disorders are a common feature of all diseases. All the clinical diseases have a nerve-endocrine-immune disorder. The disease process is actually a kind of disorder of nerve-endocrine-immune network homeostasis adjustment. however, among the nerve, endocrine and immune disorders, immune disorder is principal.Inflammatory bowel disease (IBD) is a universal chronic inflammatory disease, including chronic nonspecific ulcerative colitis (UC) and Crohn's disease (CD), The disease's distribution of is world-wide, and it seriously endangers the health of our people, and the incidence rate is increasing recently. and especially serious in Chinese, Europe and America. The key features of IBD were inflammation of intestinal tract and mucous membrane lesions. The etiology and pathogenesis of IBD are not very clear yet. The majority of researches suggest that IBD is a kind of autoimmune disease caused by the interaction of many factors including heredity, immune, environment and mucosal barrier. Among all of these, immunity plays a vital role in the occurrence and development of IBD. Many research data show that IL-6 is key factor referring to a variety of cytokines during IBD progress.In view of the above, IBD rats model was constructed by chemical induction of trinitro-benzene-sulfonic acid (TNBS). Briefly,5%TNBS and dehydrated alcohol was mixed referring to 2:1 ratio. The rats were then rectum perfused with the mixture. The rat model was sacrificed on day 3,7,14,21 and 28, and the brain and the colon tissues were stripped. The expression of IL-6 in the brain and the colon tissues was determined by immunohistochemistry and real time PCR. The regulation mechanism of the acceptor and the signal transduction factors, such as stat3, jak3, gp130, socs3, of IL-6 was identified by real time PCR. The concentration diversity of IL-6 in the serum during the treatment period was measured by ELISA. The results showed that the amount of IL-6 and its acceptors and related signal transduction factors in the intestinal change in the pathogenesis of IBD. With the development of IBD, there is a higher expression level of IL-6 and its acceptors and related signal transduction factors. When rats recovered, the expression of IL-6 and its acceptors and related signal transduction factors decreased gradually, and finally reach the normal level. The results of brain tissues were similar to the results of gut. The ELISA experiments indicated that serum IL-6 concentration heightened when have IBD, on the contrary, the serum IL-6 concentration degraded gradually accompany with disease recovery and return to the normal concentration eventually.In summary, IL-6 was the key factor in chronic phase of colonitis and its acceptors and related signals transduction factors were all involved in the development of IBD, which proved the important role of signal transduction pathway of IL-6 in the morbidity progress of IBD. The study provided the basic theory of pathogenesis research of IBD. The results also prompted that network-neuroendocrine-immune regulation network participated in the progress of IBD, which supplied the relationship research of IBD and network-neuroendocrine-immune regulation network with experimental data. |
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