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Objective: Comparative proteomics approach to screening 2,3,7,8 - tetrachlorodibenzo-p-dioxin (2,3,7,8-tetrachloro-dibenzo-p-dioxin, TCDD) caused fetal rat congenital cleft palate occurs differentially expressed proteins. Methods: ⑴ TCDD-induced congenital cleft palate model build C57BL/6J mice. Pregnancy day 12 in pregnant rats (gestational day GD) the experimental group TCDD64μg/kg gavage control group with the same amount of corn oil gavage. GD18, fetal survival rate statistics, dissecting fetal rat palate line gross anatomy and histology. (2) comparative proteomics screening TCDD-induced the fetal rat cleft palate protein. GD18, respectively, to obtain the experimental group and the control group on the fetal rat palate tissue extract total protein, two-dimensional gel electrophoresis analysis of the groups gel electrophoresis differentially expressed protein spots were obvious differences in protein spots for mass spectrometry analysis. database to retrieve identification, and validated using immunohistochemical methods related proteins have been identified. Results: ⑴ gross anatomy see, the experimental group fetal rat cleft palate incidence of 100%, the fetal rat control group palate complete. Histological observation, the experimental group on both sides of the fetal rat palate and nasal septum failed midline fusion, the formation of fissures; integration of control group on both sides of the fetal mouse palate and nasal septum contact, no epithelial raphe (midline epithelial seam, MES) mesenchymal cells are connected to each other, the integrity of the structure. (2) by two-dimensional electrophoresis, mass spectrometry and database query, the 10 kinds of the differentially expressed protein identified in the experimental group and control group, including γ-actin, a peroxide reductase 1, guanine nucleotide dissociation inhibitor malate dehydrogenase, unknown protein, galectin 7, triosephosphate isomerase, 3 - phosphate dehydrogenase, phosphoglycerate kinase, ATP synthase. Wherein the peroxide reductase 1 (peroxiredoxin 1, Prx 1) expression in the experimental group was significantly enhanced. Immunohistochemical results of Prx 1 protein in the experimental group fetal mouse palate enhanced expression, consistent with the comparative proteomic identification results. Conclusion: ⑴ TCDD can be successfully induced congenital cleft palate model to establish C57BL/6J fetal mice and molded rate of 100%, the study of the etiology and pathogenesis of cleft palate. The ⑵ peroxide reductase 1 (Prx1) significantly enhanced expression may be related to TCDD-induced fetal rat congenital cleft palate that TCDD by inducing the fetal rat oxidation emergency, Prx1 overexpression of antioxidant emergency response, thereby inhibiting the palate raised midline epithelial cells (Medial edge epithelia MEE) apoptosis side palatal normal development and mutual integration obstacles, eventually leading to the occurrence of cleft palate by fetal rat.
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