文献类型：期刊文献

中文题名：黄芪多糖对黄嘌呤氧化酶诱导的肺癌A549细胞自噬及PI3K/AKT信号通路的影响

英文题名：Effect of astragalus polysaccharide on autophagy and PI3K/AKT signaling pathway in lung cancer A549 cells induced by xanthine oxidase

作者：王雪林[1,2,3];李杨[1];刘丹[1,2,3];王彦君[1,2,3];明海霞[1,2,3,4]

第一作者：王雪林

机构：[1]甘肃中医药大学基础医学院生理教研室;[2]甘肃省高校重大疾病分子医学与中医药防治研究重点实验室;[3]甘肃中医药大学中西医结合研究所;[4]甘肃省中药药理与毒理学重点实验室,甘肃兰州730000

第一机构：甘肃中医药大学基础医学院（敦煌医学研究所）

年份：2019

卷号：35

期号：12

起止页码：1676

中文期刊名：中国药理学通报

外文期刊名：Chinese Pharmacological Bulletin

收录：CSTPCD;;Scopus;北大核心:【北大核心2017】；CSCD:【CSCD2019_2020】；

基金：甘肃省中医药管理局资助项目(No GZK-2017-6);甘肃省高等学校科研项目(No 2018A-046);甘肃省高校重大疾病分子医学与中医药防治研究重点实验室开放基金项目(No FZYX17-18-9);甘肃中医药大学研究生创新基金(No CX201833)

语种：中文

中文关键词：黄芪多糖;A549细胞;自噬;黄嘌呤氧化酶;PI3K/AKT;透射电镜

外文关键词：astragalus polysaccharide;A549 cells;autophagy;xanthine oxidase;PI3K/AKT;transmission electron microscope

摘要：目的基于PI3K/AKT信号通路观察黄芪多糖(Astragaluspolysaccharide,APS)对人肺癌A549细胞自噬的影响。方法黄嘌呤氧化酶(XOD)建立自噬模型,分别以APS(100、200、400)mg L-1浓度及3-甲基腺嘌呤(3-Methyladenine,3-MA)进行干预;CCK-8法、透射电镜及Western blot分别检测APS对人肺癌A549细胞自噬模型增殖、自噬体及自噬标记分子的影响。结果与空白组比较,模型组细胞生长加快,自噬小体数量增多,模型组LC3B及PI3K蛋白表达增高,p62及AKT降低(P<0.05);与模型组比较,APS(200、400)mg·L^-1浓度组细胞生长减慢,自噬小体数量减少,LC3B及PI3K蛋白表达下降,p62及AKT显著性增高(P<0.05);与3-MA组比较,APS(200 mg·L^-1)浓度组LC3B蛋白表达下降(P<0.05),APS(400 mg·L^-1)浓度组PI3K显著性下降(P<0.05)。结论APS可能通过下调PI3K/AKT信号通路的自噬而发挥抗肿瘤作用。
Aim To observe the regulatory effects of astragalus polysaccharide(APS)on AKT/PI3K signaling pathway in lung cancer A549 cells.Methods The autophagy model was established by xanthine oxidase(XOD).Then the intervention was carried out with 100,200,400 mg·L^-1 of APS and 3-methyladenine(3-MA).Cell Counting Kit-8(CCK-8)method,transmission electron microscope and Western blot were used to detect the effect of APS on the proliferation,autophagy and autophagy marker molecules respectively in lung cancer A549 autophagy model.Results Compared with blank group,cell growth of the model group was accelerated;the number of autophagosomes increased,and the expressions of microtubule-associated protein 1 light chain-3B(LC3B)and PI3K significantly increased,while p62 and AKT markedly decreased(P<0.05).Compared with model group,cell growth slowed down,and the number of autophagosomes decreased;the expression of LC3B and PI3K significantly decreased.However,p62 AND AKT expression significantly increased(P<0.05)in 200 or 400 mg·L^-1 of APS-treatedgroups.Compared with 3-MA-treated group,the expression of LC3B significantly decreased in 200 mg·L^-1 of APS-treated group(P<0.05),and PI3K significantly decreased in 400 mg·L^-1 of APS-treated group(P<0.05).Conclusion APS may exert anti-tumor effect by down-regulating PI3K/AKT signaling pathway of human lung cancer A549 cells.