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目的研究环磷酰胺(cyclophosphamide,CP)引起小鼠神经管畸形(neural tube defects,NTDs)的动物模型,探讨牛磺酸的保护作用及其作用机理,为预防NTDs的发生提供理论依据。方法建立CP致小鼠NTDs模型,分析比较各组鼠胚神经管发育情况和畸形情况;用免疫组织化学和图像分析技术检测各组鼠胚神经管上皮细胞中Cx26和Cx43蛋白的表达,分析其与NTDs发生的关系。结果 1)用CP建立小鼠NTDs模型的最佳剂量为15mg/kg体重,牛磺酸能有效减少NTDs的发生;2)Cx26和Cx43蛋白定位于神经细胞的胞膜和胞质,CP组Cx26和Cx43蛋白的表达明显高于对照组(P<0.05);中、高剂量牛磺酸组Cx26和Cx43蛋白的表达显著降低(P<0.05)。结论 Cx26和Cx43的过度表达可能是CP致NTDs的途径之一;牛磺酸可能拮抗CP的毒性,保护神经细胞,减少NTDs的发生。
Objective To study the animal model of neural tube defects (NTDs) caused by cyclophosphamide (CP) in mice, and to explore the protective effect of taurine and its mechanism of action to provide a theoretical basis for preventing the occurrence of NTDs. Methods CPD mouse NTDs model was established, the development and abnormality of neural tube in each group were analyzed and compared. The expression of Cx26 and Cx43 protein in neural tube epithelial cells of rats in each group was detected by immunohistochemistry and image analysis Relationship with NTDs. Results 1) The optimal dosage of CP was 15mg / kg body weight, and taurine could effectively reduce the incidence of NTDs. 2) The Cx26 and Cx43 proteins localized in the membrane and the cytoplasm of neurons, and CP group Cx26 (P <0.05). The expression of Cx26 and Cx43 protein in medium and high dose taurine group was significantly lower than that in control group (P <0.05). Conclusion Overexpression of Cx26 and Cx43 may be one of the pathways of CP-induced NTDs. Taurine may antagonize the toxicity of CP, protect nerve cells and reduce the occurrence of NTDs.