黄芪多糖对胰源性糖尿病大鼠胰腺Kir6.2表达的干预研究  

Expression of Pancreatic Kir6.2 in Pancreatogenic Diabetes Rat and the Intervention of Astragalus Polysaccharide

作　　者：陈玉涛[1] 薛承锐[1] 

机构地区：[1]天津医科大学总医院中西医结合外科,天津300052

出　　处：《医学综述》2010年第5期767-770,共4页Medical Recapitulate

摘　　要：目的观察不同剂量的黄芪多糖(APS)对胰源性糖尿病大鼠胰腺Kir6.2表达的影响。方法选择40只雄性Wistar大鼠,将其随机分为模型组、对照组、APS低剂量干预组和APS高剂量干预组。然后对4组大鼠进行口服糖耐量实验,并用反转录-聚合酶链式反应法检测4组大鼠胰腺Kir6.2mRNA和蛋白的表达水平。结果模型组大鼠胰腺Kir6.2mRNA和蛋白表达水平较对照组显著下降,高剂量组大鼠Kir6.2mRNA和蛋白的表达水平较模型组显著升高(P<0.05)。结论APS对慢性胰腺炎大鼠胰腺Kir6.2表达有一定的上调作用,可能是其发挥降糖作用的机制之一。Objective To investigate the influence of astragalus polysaccharide（APS）administration on the expression of pancreatic Kir6.2 in pancreatogenic diabetes rats.Methods Wistar rats were induced chronic pancreatitis,then divided into model group,control group,low dose group,and high dose group randomly.After oral glucose tolerance test of them were observed,determination of the Kir6.2 mRNA and protein expression levels in pancreas was performed by reverse transcription-polymerase chain reaction and Western blots.Results The expression of Kir6.2 in model group was decreased significantly,and the expressions of Kir6.2 in low dose and high dose groups were higher than that in the model group（P0.05）.Conclusion APS up-regulation to the expression of pancreatic Kir6.2,which may be a mechanism on reducing blood glucose.

关 键 词：糖尿病 慢性胰腺炎 KIR6.2 黄芪多糖 表达 

分 类 号：R587.1[医药卫生—内分泌]