摘要
目的:探讨维甲酸(RA)致神经管缺陷畸形(NTDs)的分子机理及牡蛎提取物的拮抗作用。方法:用RA建立小鼠胚胎NTDs模型,分析比较RA组、不同剂量的牡蛎保护组与各自对照组鼠胚神经管发育情况;用免疫组织化学方法和图像分析技术,对各组鼠胚的神经上皮细胞缝隙链接蛋白43(Cx43蛋白)的表达进行定性、定位和半定量观察。结果:①空白对照组和牡蛎对照组鼠胚中未见吸收胎、死胎及畸胎,神经管发育良好,Cx43蛋白定位于神经上皮细胞的细胞膜和细胞质,组间阳性表达情况比较无显著性差异(P>0.05);②RA组鼠胚吸收胎(27.2%)、死胎(5.8%)和畸胎(47.6%)发生率最高,其神经管发育不良、闭合不全,Cx43蛋白呈强阳性表达;③牡蛎高剂量组鼠胚中的吸收胎(11.6%)、死胎(3.9%)及畸胎(16.5%)均明显低于RA组(P<0.05),鼠胚神经管发育良好,与RA组比较,神经上皮中Cx43蛋白的表达显著降低(P<0.05)。结论:①Cx43蛋白的过度表达可能是RA诱导NTDs的机理之一;②牡蛎可以通过改善Cx43基因的表达而拮抗RA对胎鼠的致畸作用。
Objective：To explore the molecular mechanism of neural tube defects（NTDs） caused by retinoic acid（RA） and the antagonistic effect of oyster.Methods：Overdose RA was used to set up NTDs model in mouse embryo.Neural tube developmental condition was analyzed and compared between RA group and oyster group with each control group.An immunohistochemistry method and image analysis were employed to explore the expression of connexin43（Cx43） in the neuroepithelial of each embryo.Results：1） The neural tube in blank control group and oyster control group grew well as well as close-up at the right moment.The Cx43 positive immunostaining located not only on the membranes but also in the cytoplasms of neural epithelium.And expression of Cx43 was in the normal level.There were no significant differences in expression of Cx3 between the two groups（P0.05）.2） The embryo of mouse had the highest percentage in absorbance rate（26.9%）,death rate（5.6%） and abnormity rate（44.4%） in RA group.In RA group,neural tube developed poorly and unclosed,and Cx43 was overexpressed.3） The neural tube in RA-oyster middle-dose group and RA-oyster high-dose group grew well.And expression of Cx43 was remarkably lower than that in RA group（P0.05）.Conclusions：1）The molecular mechanism of NTDs caused by RA maybe result in the overexpression of Cx43.2） Oyster has a possible protective effect on NTDs caused by RA by down-regulae the expression of Cx43 in neuroepithelia.
出处
《生殖与避孕》
CAS
CSCD
北大核心
2011年第4期225-230,共6页
Reproduction and Contraception
