环磷酰胺致大鼠神经管畸形神经上皮细胞黏附分子和微管相关蛋白doublecortin的表达变化

Expression of neural cell adhesion molecule and doublecortin in the neuroepithelial cells of defected neural tube induced by cyclophosphamide in rats

目的：在环磷酰胺致大鼠神经管畸形（NTD）模型基础上，研究NCAM和DCX在大鼠胚胎神经上皮细胞中的表达变化，进一步探讨其致畸作用的分子机制，为预防人类神经管畸形的发生提供理论依据。方法：将孕鼠随机分实验组和对照组，应用免疫荧光技术检测NCAM和DCX在NTD发生中的表达变化。结果：给药后4、 8h，实验组NCAM和DCX阳性率与对照组相比，差异无统计学意义；给药后12、 24、 48h，实验组NCAM和DCX阳性细胞增多，NCAM和DCX阳性率与对照组相比，差异均有统计学意义。结论：环磷酰胺使NCAM、 DCX表达增加，干扰了神经元前体细胞向神经元方向的分化成熟。

Objective： On the models of neural tube defect （NTD） in rats induced by cyclophosphamide,to define the influence of cyclophosphamide on the expression of neural cell adhesion molecule （NCAM） and doublecortin （DCX） in the neuroepithelial cells, and to further explore the molecular mechanism that causes NID, which may provide a theoretical basis on the prevention of human NTD. Methods： The pregnant rats were randomly divided into an experimental group and a control group. The expressions of NCAM and DCX in the development of neural tube defect were detected using immunofluorescence labeling technology. Results： At 4, 8 hours after administration, compared with the control group, there was no significant change in the positive rate of NCAM and DCX; at 12, 24, 48 hours after administration, compared with the control group, the positive rate of NCAM and DCX in the experimental group were increased with significant differences. Conclu- sion： Cyclophosphamide can increase the expressions of NCAM and DCX, and interference the differentiation of the neuronal precursor cells to the direction of mature neurons, which may be relevant to NTD induced by cyclophosphamide.