孕鼠叶酸缺乏对新生大鼠肺发育及其表面活性蛋白C的影响

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目的寻找叶酸缺乏对大鼠肺发育影响的形态学证据,探讨肺表面活性蛋白C(SP-C)在孕鼠叶酸缺乏引起新生大鼠肺发育障碍中的作用。方法采用去叶酸RHAA配方饲料喂养大鼠,建立叶酸缺乏大鼠模型。叶酸缺乏组和对照组各18只大鼠,孕早期及孕晚期分别测定其血清叶酸水平;取各组出生14d新生大鼠右肺,常规石蜡包埋切片,用HE染色及免疫组织化学染色分别比较2组肺组织及SP-C阳性细胞的病理改变。结果叶酸缺乏组孕鼠孕早期及孕晚期血清叶酸水平均显著低于对照组(Pa<0.05),表明叶酸缺乏孕鼠模型建立成功。HE染色显示新生大鼠叶酸缺乏组肺组织结构明显被破坏;免疫组织化学染色显示,叶酸缺乏组与对照组比较,SP-C阳性的Ⅱ型细胞明显减少,黄色染色较淡,特异性显色区域较少。出生14d叶酸缺乏组新生大鼠SP-C阳性的Ⅱ型肺泡细胞免疫组织化学染色平均吸光度显著低于对照组(P<0.05)。结论孕期叶酸缺乏对新生大鼠肺发育造成一定影响,其机制可能是通过减少胎鼠肺组织SP-C的表达,进而影响肺表面活性物质的生成。 Objective To find the morphological evidence of the effect of folic acid deficiency on lung development in rats and to explore the role of lung surfactant protein C (SP-C) in the development of lung dysplasia in neonatal rats induced by folic acid deficiency in pregnant rats. Methods The rats were fed with dextran RHAA formula to establish the folate-deficient rat model. Folic acid deficiency group and control group, 18 rats respectively. The levels of serum folic acid were measured in the first trimester and the third trimester respectively. The right lungs of newborn rats on the 14th day after birth were harvested and paraffin-embedded sections were obtained. HE staining and immunohistochemical staining The pathological changes of lung tissue and SP-C positive cells in two groups were compared. Results In folic acid deficiency group, the level of serum folic acid in pregnant women in early pregnancy and the third trimester was significantly lower than that in control group (Pa <0.05), indicating that folate-deficient pregnancy model was successfully established. HE staining showed that the structure of lung tissue in neonatal rats with folic acid deficiency was obviously destroyed. Immunohistochemical staining showed that the number of type II cells with SP-C positive staining was significantly decreased compared with the control group Less area. The average absorbency of type II alveolar cells in SP-C positive neonatal rats with folate deficient 14 d after birth was significantly lower than that of the control group (P <0.05). Conclusion Folic acid deficiency during pregnancy may affect lung development in neonatal rats. The mechanism may be through the decrease of SP-C expression in fetal rat lung tissue, which may affect the generation of pulmonary surfactant.
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