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目的:探讨上皮间充质化在2，3，7，8-四氯二苯二噁英(2，3，7，8-tetrachlorodibenzo-p-dioxin，TCDD)致胎鼠腭突融合障碍中的作用。方法:将12只C57BL/6 J孕鼠按随机数字表法分为实验组和对照组，每组各6只。妊娠第10.5天(GD10.5)，实验组以28 μg/kg的TCDD(玉米油溶解)灌胃，对照组则按照等量玉米油灌胃。在GD15.5分别处死2组孕鼠，在显微镜下行胎鼠腭突的形态学观察。购买原代腭突中嵴上皮细胞进行培养，将其分为实验组和对照组，实验组细胞分为3个亚组，分别添加浓度为5、10、20 nmol/L的TCDD于培养基，对照组则使用不加TCDD的培养基。72 h后，通过免疫荧光染色、激光共聚焦检测荧光强度和蛋白质印迹法检测腭突中嵴上皮细胞标志物细胞角蛋白19(CK-19)和腭突间充质细胞标志物波形蛋白(vimentin)的表达。采用单因素方差分析法对各组数据进行比较。结果:实验组中共获得36只胎鼠，死胎和吸收胎3只，腭裂发生率为100%(33/33)，其中完全腭裂为84.8%(28/33)，部分腭裂发生率为15.2%(5/33)；对照组中获得40只胎鼠，死胎和吸收胎共2只，腭裂发生率为0(0/38)。实验组和对照组腭突中嵴上皮细胞培养72 h后形态均发生变化，由均一的鹅卵石样变为有伪足的星形或不规则形；对照组和实验组中5、10、20 nmol/L 3个亚组的腭突中嵴上皮细胞标志物CK-19蛋白相对表达量分别为0.739±0.120、0.483±0.023、1.007±0.109、1.086±0.145，荧光强度分别为53.384±5.785、36.818±8.250、64.575±8.323、76.898±3.711；腭突间质细胞标志物vimentin蛋白相对表达量分别为0.527±0.112、0.781±0.095、0.284±0.046、0.216±0.040，荧光强度分别为63.672±6.135、82.632±4.474、52.608±7.525、42.664±7.659。低剂量实验组(5 nmol/L)与对照组相比，CK-19降低而vimentin升高；高剂量实验组(10、20 nmol/L)与对照组相比，CK-19升高而vimentin降低，差异有统计学意义(n P0.05)。n 结论:腭突中嵴上皮细胞间充质化(EMT)可能是一自发程序，TCDD致腭突融合障碍可能与腭突中嵴上皮细胞EMT过程受抑制有关，且随着TCDD剂量增加，这种抑制作用保持稳定。“,”Objective:To explore the role of epithelial-mesenchymal transition(EMT) in fusion of the secondary palatal shelves to form the intact secondary palate induced by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD).Methods:Twelve C57BL/6 J pregnant mice on gestation day (GD) 10.5 were divided into two groups: one group was conducted through gastric tubes with one dose of 28 μg/kg TCDD (experimental group) and the other group was operated through gastric tubes with equal volume corn oil (control group). Embryos were removed by cesarean section from pregnant mice during the palatal formation stage (GD 15.5) and the morphology of palatal tissue was observed. Primary media edge epithelial(MEE) were divided into experimental group and control group. MEE were treated with medium containing TCDD, 5 nmol/L, 10 nmol/L, 20 nmol/L and normal medium respectively. The expression of cytokeratin 19(CK-19) protein and vimentin protein in MEE were detected by immunofluorescence laser confocal microscopy and Western blotting after 72 hours. Statistical comparisons were made using one-way ANOVA.Results:A total of 36 fetuses were obtained in the experimental group, including 3 dead fetuses and absorbed fetuses. The incidence of cleft palate was 100% (33/33); the incidence of complete cleft palate was 84.8% (28/33), and the incidence of partial cleft palate was 15.2% (5/33); 40 fetuses were obtained in the control group, including 2 dead fetuses and resorbed fetuses, and the incidence of cleft palate was 0 (0/38). After 72 hours, the shape of MEE changed from uniform pebble-like to star-like or irregular shape with pseudopodia. The expressions of CK-19 protein were(0.739 ± 0.120, 0.483 ± 0.023, 1.007 ± 0.109, 1.086 ± 0.145) and fluorescence intensities were (53.384±5.785, 36.818 ± 8.250, 64.575±8.323, 76.898 ± 3.711) in control group and TCDD (5 nmol/L), TCDD (10 nmol/L) and TCDD (20 nmol/L) groups, respectively. The expressions of vimentin protein were (0.527 ± 0.112, 0.781 ± 0.095, 0.284 ± 0.046, 0.216 ± 0.040) and fluorescence intensities were (63.672±6.135, 82.632 ± 4.474, 52.608±7.525, 42.664 ± 7.659). Compared with the control group, the low-dose experimental group (5 nmol/L) had a decrease in CK-19 and an increase in vimentin; the high-dose experimental group (10 nmol/L, 20 nmol/L) had an increase in CK-19 and a decrease in vimentin, and the expression difference was statistically significant (n P0.05).n Conclusions:EMT process of MEE was identified in vitro and was a spontaneous procedure. TCDD-induced cleft palate may be related to the inhibition of the EMT process in MEE and with the increased dose of TCDD, the effects of EMT inhibiton were sustainable.