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目的探讨妊娠合并糖尿病诱发胚胎先天性神经管缺陷的差异表达基因,揭示胚胎先天性神经管缺陷发生、发展的分子机制。方法选用2组的70～90天的SD大鼠:第1组(n=3)为接受常规饲养的正常对照组;第2组(n=3)为实验组:尾静脉注射65mg/kg链脲菌素(STZ),构建妊娠合并糖尿病诱发胚胎先天性神经管缺陷组大鼠动物模型。于妊娠第12天取出各组胚胎,解剖显微镜下进行神经管缺陷形态学判定。提取卵黄囊细胞的mRNA,以cDNA基因芯片技术对差异表达基因进行检测。结果对实验组及正常对照组卵黄囊细胞的1200个基因进行比较,共筛选出差异表达基因79条,其中42条表达上调基因(包括凋亡相关基因BAX、bcl 2、HSP70、glucose transporter3等),37条表达下调基因(包括phospholipaseA2、insulin likegrowthfactorIIreceptor等)。结论揭示了妊娠合并糖尿病诱发胚胎先天性神经管缺陷的差异表达基因,对先天性神经管缺陷有效的早期诊断和治疗提供了实验依据。
Objective To investigate differentially expressed genes in embryonic congenital neural tube defects induced by diabetes mellitus in pregnancy and to reveal the molecular mechanism of embryonic congenital neural tube defects. Methods Two groups of SD rats aged 70-90 days were selected: group 1 (n = 3) was normal control group receiving routine feeding; group 2 (n = 3) was experimental group: tail vein injection of 65 mg / kg To establish a rat model of congenital neural tube defect induced by pregnancy with diabetes mellitus (STZ). On the 12th day of gestation, each group of embryos was taken out and morphology of neural tube defects was observed under a dissecting microscope. The mRNA of yolk sac cells was extracted and the differentially expressed genes were detected by cDNA microarray. Results A total of 1200 differentially expressed genes were isolated from 1200 yolk sac cells of experimental group and normal control group. Among them, 42 genes were up-regulated (including BAX, bcl 2, HSP70 and glucose transporter3) , 37 down-regulated genes (including phospholipase A2, insulin like growth factor receptor II receptor, etc.). Conclusions The differential expression genes of congenital neural tube defect induced by pregnancy and diabetes mellitus were revealed, which provided an experimental basis for the early diagnosis and treatment of congenital neural tube defects.