Han Jing, Xiao Ying, Lin Jiu-Xiang, Zhang Zhao-Feng, Li Yong
Department of Food Science and Nutrition, School of Public Health, Peking University, Beijing 100083, China.
Wei Sheng Yan Jiu. 2006 Jan;35(1):33-5.
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 establishted.
Mouse embryonic palates were explanted on GD12 and cultured in a roller device for 72h induced by atRA in different concentrations from 10(-5) micromol/L to 10(-1) micromol/L.
Similar to development in vivo, palates in control normal fused. Compared with the control, palates development and fusion were promoted in group of 10(-15) micromol/L, while were inhibited in groups of 10(-4) micromol/L or greater, resulting in cleft palate. The proportion of fusion was reduced in a significant dose-response pattern.
In the model, the cultured palates continued developing and fusing. Palatal fusion was promoted by normally atRA in 10(-5) micromol/L level and were inhibited by atRA in 10(-4) micromol/L level or greater, which resulting in cleft palate. These mentioned confirm the validity and reliability of this model.
为研究全反式维甲酸(atRA)对小鼠腭部发育的影响及其可能机制,建立了胎鼠滚板器官培养模型。
在孕第12天取出小鼠胚胎腭部,置于滚轴装置中,用浓度从10(-5)微摩尔/升至10(-1)微摩尔/升的atRA诱导培养72小时。
与体内发育情况相似,对照组腭部正常融合。与对照组相比,10(-15)微摩尔/升组腭部发育和融合得到促进,而10(-4)微摩尔/升及以上组则受到抑制,导致腭裂。融合比例呈显著的剂量反应模式降低。
在该模型中,培养的腭部持续发育并融合。正常情况下,10(-5)微摩尔/升水平的atRA促进腭部融合,而10(-4)微摩尔/升及以上水平的atRA则抑制腭部融合,导致腭裂。上述结果证实了该模型的有效性和可靠性。