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Objective: Guillain - Barre syndrome (Guillain-Barre syndrome, GBS) is a peripheral nerve demyelination and inflammatory cell infiltration characteristics of autoimmune disease, its etiology and pathogenesis is not yet fully elucidated. Experimental autoimmune neuritis (experimental autoimmune neuritis, EAN) is a CD4 T cell-mediated peripheral nervous system demyelinating disease, because of their similar clinical and immunological characteristics with GBS and research GBS ideal model. Currently considered immune balance is broken, the generation of autoantigen-specific T cells is a key to the pathogenesis of GBS / EAN. Transforming growth factor-β1 (transforming growth factor-β1, TGF-β1) is a pleiotropic immunomodulatory TGF-β superfamily factor, function to inhibit T cell proliferation and differentiation, and in maintaining immune homeostasis play important role. Previous studies suggest that TGF-β1 is a protective factor in the GBS play immunosuppressive effects. Smads (Sma-and Mad-related proteins) in recent years, the discovery of the family provides a broad prospect for further study of the signaling pathways of TGF-p. Smads TGF-β signaling pathway, a series of intracellular transduction proteins. Now that Smad7 is a TGF-β signaling pathways important negative regulatory factors, Smad2 and Smad3 TGF-β1 receptors in the cytoplasm of the first substrate, the expression levels of Smad3 directly affect the TGF-β1 signaling. A number of studies have shown that inflammatory bowel disease, multiple sclerosis and other autoimmune diseases of Smad3 the abnormal expression associated with the expression of Smad7 molecule TGF-β/Smads signaling pathway damaged prompt of Smad3, Smad7 may interfere with the participation of the TGF-β signaling A variety of autoimmune diseases. The purpose of this experiment is to observe smad3 dynamic expression of the the smad7 protein in rat sciatic nerve in EAN to explore smad3 and the smad7 with the onset of EAN relationship, provide new therapeutic targets for the treatment of autoimmune diseases. Methods: Lewis rats of 48, male, SPF grade, 6-8 weeks, weight 160-180g, were randomly divided into: normal saline group (n = 4,4,4,4); complete Freund's adjuvant group (n = 4,4,4,4); EAN group (n = 4,4,4,4). Model: First prepare the antigen emulsion establish EAN: rats with peripheral nerve myelin protein P253-78 fully saline dissolved, with complete Freund's adjuvant (complete Freund's adjuvant, CFA) thoroughly mixed into antigen emulsion (P2 final concentration 100μg/200μL). Saline group, each rat 200μL saline instead of antigen emulsion injection; the EAN group each mouse injected 200μL antigen emulsion; adjuvant rats injected with saline and complete Freund's adjuvant, such as volume and mix 200 μL of the emulsion. Immune times are on day 0, the the immune sites were double hind foot palm subcutaneous. Incidence and pathological changes of the observed experimental rats, respectively, in the first seven days, 16 days, 24 days, 33 days the animals were killed, the pathological changes take sciatic nerve root HE staining and Weil's staining, using western blot method to detect Smad3, Smad7 protein levels. Results: 1 throughout the observation period, NS group and the adjuvant group rats asymptomatic, the weight steady growth; the EAN rats 11 days after immunization onset, reached a peak of 17 days of symptoms, basic improved to 33 days clinical score with the NS group and adjuvant group was significantly different (p lt; 0.01), the EAN rats Smad7 protein expression in the early onset of expression that is elevated compared with the NS group and the CFA group, the difference was statistically significant ( P lt; 0.01), the expression of the peak of the highest expression down the recovery period, but still significantly higher than the CFA group, NS group; 3, compared with the NS group and the CFA group, EAN rats Smad3 protein expression the onset expression were significantly lower, the difference was statistically significant (P lt; 0.05), the peak period was significantly lower (P lt; 0.01). Conclusion: 1 of Smad3 and Smad7 in the EAN dynamic expression suggesting that both may by interference TGF-β1/Smad signaling pathways involved in the pathogenesis of the EAN, Smad7, Smad3 may become a new therapeutic targets.
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