摘要
目的 探讨孕鼠肝内胆汁淤积症时胎鼠肺脏形态学和肺表面活性蛋白A（surfactantproteinA，SPA）mRNA的改变及意义。方法应用雌激素和孕激素建立妊娠期肝内胆汁淤积症大鼠模型，光镜和电镜下观察胎鼠肺组织的病理改变。采用逆转录聚合酶链反应技术检测胎鼠肺组织SP—AmRNA的表达水平。结果（1）与对照组比较，实验组胎鼠肺组织光镜下见肺间质毛细血管明显扩张、充血，大部分肺泡间隔增宽，肺泡内少量炎性渗出物，灶状肺泡内出血。电镜下见胎鼠肺泡Ⅱ型上皮细胞微绒毛减少，线粒体空泡变性，板层小体排空增多。（2）实验组胎鼠肺组织SPAmRNA的卡甘对表达量为0．71±0．10，低于对照组（1．00±0.27），差异有统计学意义（t=3．093，P〈0．05）。结论孕鼠肝内胆汁淤积症时，高胆汁酸血症对胎鼠肺组织有一定的毒性损伤作用，SPAmRNA表达下调可能参与调控胎鼠肺损伤。
Objective To investigate the pulmonary morphologic changes and pulmonary surfactant protein A （SPA） mRNA expression in fetal rats with maternal intrahepatic cholestasis of pregnancy （ICP）. Methods Animal models of intrahepatic cholestasis of pregnancy were induced by 17-α-ethinylestradiol and progesterone. Histopathologic examination of the fetal lungs was performed under light and electronic microscopes. The expression of SPA mRNA in the fetal lungs was measured by reverse transcription-polymerase chain reaction technique. Results （1） Compared with the control group, histopathologic examination showed that fetal pulmonary tissues had dilated and congested interstitial lung capillaries, thickened alveolar septum, mild focal inflammatory exudation and focal hemorrhage in alveolus. Furthermore, reduced microvilli, mitochondrion vacuolization, cytoplasm disintegration and increased lamellar body evacuation were observed in alveolar epithelial cell 1I in ICP group under light and electronic microscopes. （2） Expression of SP A mRNA in fetal lungs of ICP group （0.71±0. 10） was significantly lower than that in control group （1.00±0.27）, t= 3.093, P〈0. 05. Conclusions Hyperbileacidemia in ICP maternal rat might lead to pathological changes in fetal pulmonary tissues. Low expression of SP-A mRNA might contribute to lesions of fetal lung with ICP.
出处
《中华围产医学杂志》
CAS
2011年第5期273-276,共4页
Chinese Journal of Perinatal Medicine
