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作 者:周晓红[1] 杨雪[1] 连蕾[1] 冯志星[1] 要兆旭[1] ZHOU Xiaohong;YANG Xue;LIAN Lei;FENG Zhixing;YAO Zhaoxu(Department of Otolaryngology,Handan Central Hospital,Handan 056000,China)
机构地区:[1]邯郸市中心医院耳鼻喉科,河北邯郸056000
出 处:《标记免疫分析与临床》2022年第2期236-241,共6页Labeled Immunoassays and Clinical Medicine
基 金:河北省医学科学研究重点课题计划项目(编号:20181672)。
摘 要:目的研究白芍总苷(TGP)对喉癌Hep-2细胞增殖、侵袭和迁移能力的影响,并初步探究磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)/糖原合成酶激酶3β(GSK3β)信号通路在此过程中的作用。方法体外培养喉癌Hep-2细胞,设对照组、25μg/mL TGP组、50μg/mL TGP组、100μg/mL TGP组,采用不同浓度TGP(0、25、50、100μg/mL)作用后,分别采用细胞计数试剂盒8(CCK-8)、Transwell法、划痕实验检测喉癌Hep-2细胞增殖活力、侵袭能力、迁移能力,蛋白免疫印迹法检测喉癌Hep-2细胞中PI3K/Akt/GSK3β信号通路相关蛋白表达水平。结果与对照组相比,25、50、100μg/mL TGP组喉癌Hep-2细胞增殖活力、侵袭能力、划痕闭合率和磷酸化PI3K(p-PI3K)、磷酸化Akt(p-Akt)、磷酸化GSK3β(p-GSK3β)蛋白表达水平显著降低(P<0.05),均呈现浓度依赖性(P<0.05)。结论TGP能够抑制喉癌Hep-2细胞增殖、侵袭、迁移,其机制可能与抑制PI3K/Akt/GSK3β信号通路表达有关。Objective To study effects of total glucosides of paeony(TGP)on the proliferation,invasion and migration of laryngeal cancer Hep-2 cells,and to explore phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/glycogen synthase kinase 3β(GSK3β)for their roles in this signaling pathways.Methods Laryngeal cancer Hep-2 cells were cultured in vitro.The control group,25μg/mL TGP group,50μg/mL TGP group and 100μg/mL TGP group were treated with different concentrations of TGP(0,25,50 and 100μg/mL).Cell counting kit 8(CCK-8),trans-well method,and scratch test were used to detect the proliferation activity,invasion ability,and migration ability of laryngeal cancer Hep-2 cells,and western blot was conducted to detect laryngeal cancer Hep-2 cells PI3K/Akt/GSK3βsignal pathway related-proteins expression levels.Results Compared with the control group,the proliferation activity,invasion ability,scratch closure rate and the expression levels of phosphorylated PI3K(p-PI3K),phosphorylated Akt(p-Akt)and phosphorylated GSK3β(p-GSK3β)in(25,50,100μg/mL)TGP group laryngeal cancer Hep-2 cells decreased significantly in a concentration dependent manner(P<0.05).Conclusion TGP could inhibit the proliferation,invasion and migration of laryngeal cancer Hep-2 cells,and its mechanism could be related to the inhibition of PI3K/Akt/GSK3βsignal pathway expression.
关 键 词:白芍总苷 喉癌HEP-2细胞 增殖活力 侵袭能力 划痕闭合率 磷脂酰肌醇3-激酶/蛋白激酶B/糖原合成酶激酶3β信号通路
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