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目的 研究环磷酰胺致大鼠胚胎神经管畸形的作用及可能机理 ,并为其防治奠定基础。方法 将大鼠按体重随机分为正常对照组及 4个不同剂量的实验组 ,其剂量分别为 7 5 ,10 5 ,12 5和 15mg/kg ,均于孕 13天腹腔一次性注射相应剂量的环磷酰胺 ,于孕 14天各组随机处死 3只 ,胎鼠进行光镜形态学观察 ;其余动物均于孕 2 0天时处死 ,进行孕鼠血清生化指标的检测、胎鼠外形及病理检测和骨骼标本的观察。结果 胎鼠神经管畸形发生率及颅骨缺损、孕鼠血清的MDA、NO含量与环磷酰胺的剂量呈正相关 ;孕鼠血清的SOD、胎鼠的生长发育指标与剂量呈负相关 ;胎鼠畸形发生处有大量的凋亡细胞存在 ;以 12 5mg/kg的剂量组致畸率高且致死率低。 结论 利用环磷酰胺制备大鼠神经管畸形模型以 12 5mg/kg的剂量效果最佳 ;畸形的发生与孕鼠机体抗氧化能力降低及胚胎神经管细胞过度凋亡有关
Objective To study the role and possible mechanism of cyclophosphamide induced neural tube defects in rat embryos and lay a foundation for its prevention and treatment. Methods The rats were randomly divided into normal control group and 4 different doses of experimental group according to their body weight. The doses were 75, 105, 125 and 15 mg / kg respectively. All the rats were injected intraperitoneally with the corresponding dose Cyclophosphamide, 14 mice in each group were randomly sacrificed on the 14th day of gestation. Fetal mice were observed morphologically by light microscopy. The other animals were sacrificed at 20 days of gestation. Serum biochemical markers, Observation of skeletal specimens. Results The incidence of fetal neural tube defects and skull defects in fetal rat embryos, serum MDA and NO levels were positively correlated with the dose of cyclophosphamide; serum SOD, fetal growth and development indicators and dose was negatively correlated; fetal malformation Occurrence of a large number of apoptotic cells exist; 125mg / kg dose group of high teratogenicity and low lethality. Conclusion Cyclophosphamide is the best choice for rat model of neural tube defects at dose of 125 mg / kg. The deformity is related to the decrease of antioxidant capacity and excessive apoptosis of embryonic neural tube cells