全反式视黄酸诱发胎鼠腭裂及抑制Smad2磷酸化的作用  

Inhibition of pSmad implicated in cleft palate induced by all-trans retinoic acid

作　　者：刘小转[1] 张航[2] 许燕[1] 韩雪飞[1] 鄢文海[1] 邢莹[1] 余增丽[2] 

机构地区：[1]郑州大学基础医学院,郑州450001 [2]郑州大学公共卫生学院

出　　处：《卫生研究》2009年第2期136-138,共3页Journal of Hygiene Research

基　　金：国家自然科学基金资助项目(No.30500540)

摘　　要：目的观察过量全反式视黄酸(atRA)对胎鼠腭发育的影响及其对Smad2磷酸化的调节作用。方法将ICR孕鼠随机分为atRA实验组和溶剂对照组,在11天(查见阴栓为孕0天),分别灌胃给予80mg/(kg·d)atRA或等体积的玉米油溶剂。常规HE组织学染色观察胎鼠上腭发育情况;免疫组化和Western Blot检测突中嵴上皮内pSmad2的表达。结果80mg/(kg·d)atRA可导致90%胎鼠发生腭裂;在腭突融合过程中,中嵴上皮细胞内Smad2被内源性的激活,出现明显磷酸化,在80mg/(kg·d)atRA组,可检测到总Smad,但是不能检测到磷酸化pSmad2的表达。结论孕期过量atRA可导致胎鼠发生腭裂,其致畸作用机制可能与中嵴上皮细胞内Smad2磷酸化被抑制有关。Objective To investigate the effects of excessive all-trans retinoic acid （atRA） on palatogenesis in mouse fetuses and level of Smad2 phophorylation （pSmad2）. Methods atRA （80mg/kg· d） was orally given to mice on embryonic day 11 （Ell）. Palatal fusion was examined by Hemagglutinin Esterase （HE）. The level of Smad2 phophorylation （pSmad2） in medial edge epithelial （MEE） was detected by immunohistochemistry and Western Blot, respectively. Results The incidence of cleft palate （CP） was 90% of total fetus in atRA-treated group. Compared with vehicle control group, no pSmad2 was identified in MEE in atRA-treated palatal shelves, which was correlated with the persistence of the MEE and failure of palatal fusion. Conclusion Inhibition of Smad phosphorylation might be involved in cleft palate induced by atRA. Key words：cleft palate, all-trans retinoic acid （atRA）, Smad2 phosphorylation （pSmad2）

关 键 词：腭裂 全反式视黄酸 pSmad2 

分 类 号：Q562[生物学—生物化学] Q132.7