文献类型：期刊文献

中文题名：黄芪甲苷对特发性肺纤维化模型大鼠肺组织CD34表达的影响

英文题名：Effects of Astragaloside Ⅳ on the Expressions of Lung Tissue CD34 of Rat Model with Idiopathic Pulmonary Fibrosis

作者：李红[1,2,3];沈明霞[1];谢海彬[2];缪天玲[2];冯玉平[4];王胜武[5];邓海娟[1]

第一作者：李红

机构：[1]甘肃中医药大学附属医院,甘肃兰州730020;[2]甘肃中医药大学;[3]甘肃省中医药防治慢性病重点实验室;[4]兰州兰石医院;[5]武威市中医医院

第一机构：甘肃中医药大学第二附属医院

年份：2015

卷号：28

期号：9

起止页码：6

中文期刊名：西部中医药

外文期刊名：Western Journal of Traditional Chinese Medicine

收录：CSTPCD

基金：甘肃省中医药科学技术研究立项资助课题(编号GZK-2011-19)

语种：中文

中文关键词：特发性肺纤维化;黄芪甲苷;CD34

外文关键词：idiopathic pulmonary fibrosis; astragaloside Ⅳ; CD34

摘要：目的:观察黄芪甲苷对特发性肺纤维化(IPF)模型大鼠肺组织CD34表达的影响,为其临床应用提供依据。方法:采用气管穿刺快速推注博来霉素法复制大鼠肺纤维化模型。将SPF级Wistar大鼠按照随机数字表法分为空白组,模型组,激素组,黄芪甲苷高、中、低剂量组,每组12只。造模后第2日起灌胃干预各组大鼠,于灌胃后第7、14、28天,采用免疫组化结合图像分析处理系统,比较CD34在各组大鼠肺组织中的表达。结果:模型组肺组织CD34的表达在7、14、28天较同期空白组增强(P<0.05);黄芪甲苷组、激素组表达较同期模型组明显减弱(P<0.01);黄芪甲苷高、中剂量组肺组织CD34的表达较激素组减弱(P<0.05);低剂量组表达与激素组比较无差异(P>0.05)。结论:黄芪甲苷可以抑制特发性肺纤维化模型大鼠肺组织CD34的表达,其干预效果与剂量及时间呈正相关。
Objective： To provide the evidence for clinical application and development of astragaloside Ⅳ by observing the effects of astragaloside IV on CD34 expressions in lung tissue of rat model with idiopathic pulmonary fibrosis （IPF）. Methods： IPF rat model was established by the method of tracheal aspiration and syringe pump of bleomycin. Wistar rats were divided into the blank group, the model group, hormone group, high, moderate and low doses groups of astragaloside Ⅳ, 12 rats each group. The rats were intervened by intragastric administration at the second day after establishing the models; the system was analyzed and dealt with immunohistochemical tests and the images at the seventh day, 14th day and 28th day after intragastric administration to compare the expressions of CD34 in the lung tissue of the rats in different groups. Results： CD34 expressions in the lung tissue of the rats in the model group were enhanced at the seventh day, 14th day and 28th day compared with the blank group at the same time （P〈0.05）; astragaloside Ⅳ groups and hormone group decreased obviously compared with the expressions of the model group at the same time （P〈0.01）; high and moderate doses groups of astragaloside IV reduced compared with hormone group in CD34 expressions （P〈0.05）; there was no difference in the comparison of the CD34 expressions between low doses group and hormone group （P〈0.05）. Conclusion： Astragaloside Ⅳ could inhibit CD34 expressions of lung tissue of rat model with IPF, and its effects are positively related to the dosage and time.