摘要
目的:探讨bcl-2在正常神经管发育和异常神经管缺陷中的作用。方法:构建了重组bcl-2的真核表达载体,建立了维A酸致小鼠神经管缺陷(neuraltubedefects,NTD)模型。用全胚胎培养结合显微注射技术将重组的正义bcl-2表达质粒导入NTD鼠胚后,观察神经管缺陷的改善程度。结果:经转染bcl-2基因后,前脑的关闭率由原来的34%增至80%,中脑的关闭率由原来的17%增至70%,后脑的关闭率也由原来的25%增至增加了70%,脊神经管的关闭率达到100%。结论:RA介导的神经管缺陷可部分被重组的bcl-2基因缓解。
AIM: To explore the role of bcl 2 in the normal development of neural tube and abnormal neural tube defect (NTD). METHODS: In present study the eukaryotic expressive vector of the recombination bcl 2 was reconstructed and neural tube closure defect (NTCD) mouse model induced by retinoic acid (RA) was established.After the recombination sense Bcl 2 mRNA was microinjected into embryos of NTCD model through the yolk sac in whole embryo culture,the improvement of NTD and apoptosis of neuroepithelial cells were observed. RESULTS:NTCD mouse model was successfully induced by RA and it was found that RA at a dosage of 50 km/kg was more suitable for inducement of NTCD model.After bcl 2 gene was transfected,the closure rate of forebrain was increased from 34%to 80%,from 17%to 70%for midbrain and from 25%to 70%for hindbrain.Simultaneously,the closure rate of spinal neural tube reached 100%. CONCLUSION:bcl 2 is involved in the regulation of the neural tube development.
出处
《中国临床康复》
CSCD
2003年第32期4357-4358,共2页
Chinese Journal of Clinical Rehabilitation
基金
国家自然科学基金资助课题(39970768)
教育部高校骨干教师基金资助~~