0 ± 16.1 vs 47.9 ± 6.3, 51.2 ± 6., P < 0.05). (3)The expression

of GHR and IGF-1R in the epiphyseal growth plate: GHR expressed in the entire epiphyseal growth plate area, but according to the immunohistochemical sections it mainly expressed in resting zone. The strong positive expression cells count of 4 different enteral nutrition model groups had no significant difference (P > 0.05) at 7th day. Conclusion: The peptide-based formula seems to be the best in promoting the expression of IGF-1 and IGFBP3, and accelerate the growth of long bones within 7 days after operation. Key Word(s): 1. IBD; selleck compound 2. nutrition; 3. animal model; 4. growth factors; Presenting Author: SHENGNAN WANG Additional Authors: YING HUANG, YING KIT LEUNG Corresponding Author: YING HUANG Affiliations: Children’s Hospital of Fudan University; Fudan University Children’s Hospital Objective: Thalidomide has anti-angiogenesis and anti-TNF-alpha pharmacological effects and is being used in the treatment small molecule library screening of refractory Crohn’s disease. It is the objective of this study to explore the role of thalidomide on the regulation of tight junction proteins in a TNBS-induced inflammatory bowel disease rat

model; and further elucidate the mechanism of thalidomide’s effect on the intestinal mucosa barrier. Methods: Methods80 Sprague-Dawley rats of 4–5 weeks old were divided into control group (24 rats), model group (28 rats, TNBS

150 mg/kg) and treatment group (28 rats, thilomide150 mg/kg). 8–12 rats were sacrificed in each group on the 7th day and 10th day; and specimens from blood and colon were studied: (1)electron microscopy, general scoring, histological injury scoring; (2) TNF-a levels in blood; (3) Western blot and PCR to evaluate the expression of occludin and claudin-1; (4) Immunohistochemistry and PCR to observe ZO-1 expression and location. Results: Intracolonic administration of TNBS can cause TNF-a level elevated in blood, with severe inflammation in the mucosa and submucosa with infiltration of neutrophils. At the nearly same time, the structure of tight junctions will be destroyed, with increased dephosphorylated occludin, reduced claudin-1 protein and zo-1 redistributed to the cytoplasm. intracolonic administration of TNBS can cause increased expression of occluding and zo-1, and decreased expression of claudin-1. Treatment with thalidomide can significantly reduce the level of blood TNF-a, and reduce the inflammatory cellular infiltration; and improve the orderly arrangement of epithelial cells and intestinal tight junctions. Compared with the model group, dephosphorylated occludin was reduced, while claudin-1 protein was increased; and the quantity of zo-1 beside the cell membrane was increased.