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作 者:何苇[1,2] 李承浩[1,2] 卢胜军[1,2] 蒙田[1,2] 石冰[1,2]
机构地区:[1]四川大学口腔疾病研究国家重点实验室,四川成都610041 [2]四川大学华西口腔医院唇腭裂外科
出 处:《口腔医学研究》2009年第1期8-11,共4页Journal of Oral Science Research
基 金:国家自然科学基金重点资助项目(编号:30530730)
摘 要:目的:观察地塞米松和维生素B12作用后腭胚突超微结构的变化。方法:将孕鼠分为实验组(致畸组,拮抗组)和对照组,按体重分别注射地塞米松、地塞米松+维生素B12和生理盐水,分别在E14.5 d和E17.5 d处死孕鼠并获取胚胎,用扫描电镜观察E14.5 d的腭胚突表面结构,记录E17.5 d腭胚突的腭裂情况。结果:地塞米松作用后,小鼠胚胎的腭裂发生率从3.1%上升到42.1%(P<0.01),硬腭处细胞的伪足结构消失。维生素B12拮抗后,小鼠胚胎的腭裂发生率降低(P<0.05),伪足结构部分恢复。结论:维生素B12能部分恢复小鼠腭胚突细胞的表面超微结构,从而拮抗地塞米松的致腭裂效应。Objective: To observe the alteration of mouse embryonic palatal uhrastructure after DEX and Vitamin B12 exposure. Methods : Dams were divided into experimental group and control group and were injected with DEX, DEX + Vitamin B12 and NS by weight, respectively. Dams were killed and fetus were collected at El4.5 and 17.5. We observed surface structure of mouse embryonic palate with SME and recorded the number of cleft palate. Results: Incidence of cleft palate increased from 3.1% to 42.1% and filopodia disapperaed in hard palate when DEX treated. After Vitamin B12 treatment, incidence of cleft palate decreased and filopodia recoved to some extent. Conclusion: Vitamin B12 restrained cleft palate induced by DEX and recoved uhrastructure of mouse embryonic palate imcompeletely.
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