汉防己甲素对先天性膈疝大鼠模型胎仔肺内表皮生长因子及其受体的影响和意义  

EFFECT AND SIGNIFICANCE OF TETRANDRINE ON EPIDERMAL GROWTH FACTOR AND ITS RECEPTOR IN THE LUNG OF CONGENITAL DIAPHRAGMATIC HERNIA RAT MODEL

作　　者：王永刚[1] 刘文英[1] 林涵[1] 熊中讯[1] 彭强[1] 王勇[1] 

机构地区：[1]四川大学华西医院小儿外科

出　　处：《中国修复重建外科杂志》2006年第11期1109-1113,共5页Chinese Journal of Reparative and Reconstructive Surgery

摘　　要：目的探讨中药成分汉防己甲素(tetrandrine,TET)对大鼠先天性膈疝(congenitaldiaphragmatichernia,CDH)模型胎仔肺内表皮生长因子(epidermalgrowthfactor,EGF)及其受体(epidermalgrowthfactorreceptor,EGFR)的影响和意义。方法实验组20只雌性SD大鼠于孕9.5d灌胃给予除草醚115mg/只;对照组4只灌胃给等量食用油。孕18.5d,实验组根据给药不同随机分为生理盐水组(normalsolutiongroup,NS组)、地塞米松组(dexamethasonegroup,Dex组)、汉防己甲素组(tetrandringegroup,TET组)、地塞米松+汉防己甲素组(D+T组),每组5只。孕21.5d对所有孕鼠行剖宫产,取出胎鼠两侧肺组织行大体观察、HE染色、EGF、EGFR免疫组织化学染色和图像分析。结果正常对照组共产胎仔36只,无隔疝形成。实验组共产胎仔137只,CDH形成64只,致畸率46.7%。在Dex组、TET组和T+D组,肺组织处于原始肺泡期或进一步成熟。EGF在NS组、Dex组、TET组、D+T组及对照组的表达量依次递减(P<0.05),而EGFR在NS组、Dex组、TET组、D+T组和对照组的表达量依次递增(P<0.05)。结论TET可使CDH胎鼠肺内EGF表达高峰提前,使EGFR表达上调,TET和Dex联合作用对促进EGF表达高峰提前及EGFR表达上调具有明显的协同效应。TET可以通过调节EGF及EGFR在肺内的表达而实现其促进肺组织细胞发育分化和改善肺血管构型的效应。Objective To investigate the effect of the traditional Chinese medicine ＂Tetrandrine＂（TET） and its significance on epidermal growth factor （EGF） and its receptor （EGFR） in the lung of nitrofen-induced congenital diaphragmatic hernia（CDH） rat model. Methods Twenty female rats were given maternal administration of a single oral dose （115 mg/rat） of nitrofen to induce CDH at 9. 5 days after pregnancy and were divided into normal solution group（NS, n=5）, dexamethasone group （Dex, n=5）, tetrandrine group （TET, n=5） and Dex＋TET group（n= 5） at 18.5 days; 4 rats were given edible oil as controls. All fetuses were delivered by cesarean section at 21.5 days. Lung histologic evaluations and EGF, EGFR immunohistochemical staining and image analysis were performed. Results CDH was observed in 64 of the 137 rat fetuses （46.7%） in the experimental groups; no CHD was observed in 36 rat fetuses of control group. The lungs of CDH fetuses showed marked hypoplasia in NS group, in contrast to improved mesenchymal differentiation in that of Dex, TET, Dex＋TET groups. The expression of EGF was weaker and weaker and that of EGFR was stronger and stronger as following order： NS, TET, DEX, T＋D and control groups; showing significant differences between them （P〈0. 05）. Conclusion Prenatal TET administration shows marked improvement in pulmonary hypoplasia through pre-regulating crest-time of EGF expression and up-regulating EGFR expression in the lungs of nitrofen-induced CDH rat model. A combination of TET and Dex would generate evident synergistic effect.

关 键 词：肺发育 先天性膈疝 表皮生长因子 汉防己甲素 动物模型 

分 类 号：R285[医药卫生—中药学] R726.5[医药卫生—中医学]