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作 者:韩静[1] 肖颖[1] 林久祥[2] 张召锋[1] 李勇[1]
机构地区:[1]北京大学公共卫生学院营养与食品卫生学系,北京100083 [2]北京大学口腔医院
出 处:《卫生研究》2006年第1期33-35,共3页Journal of Hygiene Research
基 金:国家"973"项目(No.2001CB510305);国家自然科学基金(No.30371224;30371559)
摘 要:目的为研究全反式视黄酸(atRA)对小鼠腭板发育的影响及其致腭裂的机制,建立腭板旋转培养模型。方法于妊娠第12天取下小鼠胚胎腭移植体,以10-5~10-1μmolLatRA诱导,在旋转培养装置中连续培养72h,观察腭板发育融合情况。结果经72h培养后,对照组正常融合,与体内发育一致。atRA在10-5μmolL能促进腭板的融合,≥10-4μmolL抑制腭板的发育及融合,造成腭裂,融合率下降,并呈显著的剂量-效应关系。结论本模型中,腭板能在体外培养中存活并继续生长、发育、融合;atRA在10-5μmolL能促进腭板融合,高于10-4μmolL呈剂量-效应关系的抑制融合,造成腭裂,证明小鼠腭板旋转培养模型建立成功。Objective To investigate the effect of all-trans retinoic acid (atRA) on the development of mouse palates and its possible mechanism, a model of fetal mouse rolling plate organ culture was establisbted. Methods Mouse embryonic palates were explanted on GDu and cultured in a roller device for 72h induced by atRA in different concentrations from 10^-5μmol/L to 10^-1μmol/L. Results Similar to development in vivo, palates in control normal fused. Compared with the control, palates development and fusion were promoted in group of 10^-5μmol/L, while were inhibited in groups of 10^-4μmol/L or greater, resulting in cleft palate. The proportion of fusion was reduced in a significant doseresponse pattern. Conclusion In the model, the cultured palates continued developing and fusing. Palatal fusion was promoted by normally atRA in 10^-5μmol/L level and were inhibited by atRA in 10^- 4μmol/L level or greater, which resulting in cleft palate. These mentioned confirm the validity and reliability of this model.
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