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作 者:王永刚[1] 刘文英[1] 翟春宝[1] 熊中讯[1] 魏艇[1] 唐耘熳[1]
机构地区:[1]四川大学华西医院小儿外科,成都现在山西省人民医院工作610041
出 处:《中华小儿外科杂志》2005年第6期322-325,共4页Chinese Journal of Pediatric Surgery
摘 要:目的观察表皮生长因子(EGF)及其受体(EGFR)在Nitrofen诱导的CDH模型胎肺中表达的情况,探讨CDH时肺发育不良的原因。方法实验组20只SD怀孕大鼠于孕9.5d时经胃管给予Nitrofen,正常对照组给食用油,孕21.5d时对所有孕鼠行剖宫产,取出胎鼠两侧肺组织进行EGF和EGFR免疫组化染色和图像分析。结果实验组死亡1只,致畸率46.7%;CDH肺发育不良,处于假腺体期和原始肺小管期,EGF表达上调而EGFR表达下调(P<0.05),膈疝侧与非膈疝侧肺组织EGF及EGFR表达差异没有统计学意义(P>0.05);实验组内产生CDH者胎肺内EGF和EGFR表达与无CDH者相差不大(P>0.05)。结论大鼠CDH模型中,腹腔内器官进入胸腔对肺组织的压迫可能并不是肺发育不良的主要原因,肺发育不良于膈疝形成前就已发生。CDH肺发育不良与EGF EGFR系统的变化密切相关。Objective The objective of the study is to evaluate the expression of epithelial growth factor (EGF) and epithelial growth factor receptor (EGFR) in rat lungs with nitrofen-induced pulmonary hypoplasia. Methods CDH was induced in Sprague-Dawley rats by gavaging time-pregnant mice with a single dose of nitrofen (115mg/kg) at E (9.5.) Oil was administered to the control group. All fetuses were delivered by Cesarean section on day (21.5. )Lung histology and EGF, EGFR immunohistochemistry staining were performed, and the image analyzed. Results CDH was detected in 64 out 137 rat fetuses examined ((46.7%)). The lungs of CDH fetuses showed marked hypoplasia, in contrast to those of control (P<(0.05)). There was no significant difference in EGF and EGFR expressions between the lungs with CDH and those without (P>(0.05)), neither was there any difference between the lungs from CDH side and non- CDH side (P>(0.05)).Conclusions Lung compression by herniated viscera is unlikely to cause of pulmonary hypoplasia in nitrofen-induced CDH rat model.
关 键 词:肺发育不良 先天性膈疝 表皮生长因子(EGF) 受体 肺内 鼠胎 免疫组化染色 EGFR表达 CDH 正常对照组 实验组 肺组织 图像分析 表达下调 表达上调 表达差异 经胃管 孕大鼠 食用油 剖宫产 统计学 腹腔内 模型
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