文献类型：期刊文献

中文题名：黄芪对急性肺损伤大鼠模型肺组织中角质细胞生长因子表达的影响

英文题名：Effect of Huangqi on KGF in rats with ALI

作者：赵敏[1];师霞[1];邱桐[1];翟健宇[1]

第一作者：赵敏

机构：[1]甘肃中医学院,甘肃兰州730000

第一机构：甘肃中医药大学

年份：2013

卷号：5

期号：5

起止页码：11

中文期刊名：中医临床研究

外文期刊名：Clinical Journal Of Chinese Medicine

语种：中文

中文关键词：黄芪;急性肺损伤;油酸;角质细胞生长因子;肺泡Ⅱ上皮细胞

外文关键词：Huangqi; ALl; Oleic acid; Keratinocyte growth factor; Ilalveolar epithelial cells

摘要：目的:研究黄芪对急性肺损伤大鼠肺组织中角质细胞生长(Keratinocyte GrowthFactor,KGF)表达的影响,并探讨其可能的机制。方法:SPF级Wistar大鼠60只,随机分为正常对照组(Normal Saline,NS组)、模型组(Acute Lung Injury,ALI组)、黄芪高剂量组(large does of astragalus membranaceous)、黄芪中剂量组(middle does of astragalus membranaceous)、黄芪低剂量组(small does of astragalus membranaceous)、地塞米松组(Dexamethasone,DEX组)。通过静脉内注射油酸(Oleic Acid,OA)0.1mlkg-1建立大鼠模型,利用光镜观察肺部组织形态学变化,计算肺系数(Lung Index,LI),酶联免疫吸附法(ELISA)测定血清中KGF含量,采用实时荧光定量PCR法检测肺组织KGFmRNA表达情况。结果:黄芪高、中剂量能提高血清KGF含量(P<0.01),降低肺系数(P<0.01),增强肺组织KGFmRNA表达(P<0.05),减轻肺组织病理损伤。黄芪低剂量的效果不如高、中剂量(P<0.05)。结论:黄芪能够明显减轻油酸所致急性肺损伤的炎症反应,其药理作用机制与上调肺内KGF的表达,从而刺激肺泡Ⅱ上皮细胞(ⅡAlveolar EpithelialType Cells,AECII)增生有关。
Objective： To investigate the effect and mechanism of Huangqi on acute lung injury （ALl） rat induced by OA. Methods： 60 SPF Wistar rats were randomly divided into 6 groups, control group, model group, LA group, MA group, SA group and dexamethasone goup. A rat model of ALI was established by intravenous injection of oleic acid with a dose of 0.1mlokg-1. Light microscope was used to examine hist0!ogical changes and lung index was calculated by weighting method. KGF levels in serum were determined using commercial enzyme-link,,ed immunosorbent assay kits. The expression of KGF genes were detected by real-time PCR. Results： LA group and MA group improved thproduction of KGF in whole blood （P〈0.01）, reduced the lung index （P〈0.01） and intensified KGFm RNA expression （P〈0.05） as compe with the ALl group Pathological changes of ALI were reduced significantly in AM intervention groups. SM group was lower than the effect of LA group and MA group （P〈0.05）. Conclusion： Huangqi could alleviate oleic acid induced acute lung injury in rats, and its pharmacological action mechanism may be related to raise the lungs KGF expression, so as to stimulate II alveolar epithelial type cells （AECII） proliferation.