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胡黄连苷Ⅱ通过MEK/ERK通路抑制食管癌细胞增殖及侵袭转移的机制研究 被引量:4

Mechanism of Picroside Ⅱ Inhibiting Proliferation,Invasion and Metastasis of Esophageal Cancer Cells Through MEK/ERK Pathway
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摘要 目的:探讨胡黄连苷Ⅱ通过丝裂原活化的细胞外信号调节激酶(mitogen extracellular signal regulated kinase,MEK)/细胞外信号调节激酶(extracellular signal regulated kinase,ERK)通路抑制食管癌Eca109细胞增殖及侵袭转移的作用机制。方法:将人食管癌细胞Eca109分为正常培养组(常规培养)、胡黄连苷Ⅱ组(20μmol/L胡黄连苷Ⅱ)、激活剂组(20μmol/L MEK/ERK信号通路激活剂)以及胡黄连苷Ⅱ+激活剂组(20μmol/L胡黄连苷Ⅱ培养液+20μmol/L MEK/ERK信号通路激活剂)。以四唑盐法检测四组Eca109细胞增殖活性,以流式细胞仪检测四组Eca109细胞凋亡及周期情况,以Transwell小室、划痕实验检测细胞侵袭及迁移能力,以蛋白免疫印迹法检测细胞凋亡相关蛋白、周期相关蛋白以及MEK/ERK通路相关蛋白表达情况。结果:与正常培养组相比,胡黄连苷Ⅱ组细胞增殖抑制率、细胞凋亡率,Caspase-3、Bax蛋白表达,G0/G1期、S期比例升高;Bcl-2蛋白,G2/M期比例,侵袭细胞数、划痕愈合率,细胞周期相关蛋白、MEK/ERK通路相关蛋白表达降低,上述差异均有统计学意义(P<0.05)。与正常培养组相比,激活剂组细胞增殖抑制率、细胞凋亡率,Caspase-3、Bax蛋白表达,G0/G1期、S期比例降低;Bcl-2蛋白,G2/M期比例,侵袭细胞数、划痕愈合率,细胞周期相关蛋白、MEK/ERK通路相关蛋白表达升高,上述差异均有统计学意义(P<0.05)。与胡黄连苷Ⅱ组相比,胡黄连苷Ⅱ+激活剂组细胞增殖抑制率、细胞凋亡率,Caspase-3、Bax蛋白表达,G0/G1期、S期比例降低;Bcl-2蛋白,G2/M期比例,侵袭细胞数、划痕愈合率,细胞周期相关蛋白、MEK/ERK通路相关蛋白表达升高,上述差异均有统计学意义(P<0.05)。与激活剂组相比,胡黄连苷Ⅱ+激活剂组细胞增殖抑制率、细胞凋亡率,Caspase-3、Bax蛋白表达,G0/G1期、S期比例升高;Bcl-2蛋白,G2/M期比例,侵袭细胞数、划痕愈合率,细胞周期相关蛋白、MEK/ERK通路相� OBJECTIVE:To probe into the mechanism of picroside Ⅱ inhibiting proliferation,invasion and metastasis of esophageal cancer Eca109 cells through mitogen extracellular signal regulated kinase(MEK)/extracellular signal regulated kinase(ERK)pathway.METHODS:Human esophageal cancer cells Eca109 were divided into normal culture group(conventional culture),picroside Ⅱ group(20μmol/L of picroside Ⅱ),activator group(20μmol/L of MEK/ERK signaling pathway activator)and picroside Ⅱ+activator group(20μmol/L of picroside Ⅱ+20μmol/L of MEK/ERK signaling pathway activator).The proliferative activity of Eca109 cells in each group was detected by tetrazolium salt method,the apoptosis and cycle of Eca109 cells in each group were detected by flow cytometry,the cell invasive and metastasizing ability were detected by Transwell and scratch assay,the expression of apoptosis-related proteins,cycle-related proteins and MEK/ERK pathway-related proteins were detected by protein immunoblotting.RESULTS:Compared with the normal culture group,the inhibition rate of cell proliferation,apoptosis rate,Caspase-3 and Bax protein expression,G0/G1 phase and S phase ratio were increased in the picroside Ⅱ group;the Bcl-2 protein,G2/M phase ratio,invasion cell number,scratch healing rate,cell cycle-related proteins and MEK/ERK pathway-related proteins of picroside Ⅱ group were decreased,with statistically significant differences(P<0.05).Compared with the normal culture group,the inhibition rate of cell proliferation,apoptosis rate,Caspase-3 and Bax protein expression,G0/G1 phase and S phase ratio were decreased in the activator group;the Bcl-2 protein,G2/M phase ratio,invasion cell number,scratch healing rate,cell cycle-related proteins and MEK/ERK pathway-related proteins of the activator group were significantly increased,with statistically significant differences(P<0.05).Compared with the picroside Ⅱ group,the inhibition rate of cell proliferation,apoptosis rate,Caspase-3 and Bax protein expression,G0/G1 phase and S phase ratio we
作者 杨谦 张军 马玉泉 谭雪敏 YANG Qian;ZHANG Jun;MA Yuquan;TAN Xuemin(Dept.of Thoracic Surgery,Handan Central Hospital,Hebei Handan 056000,China)
出处 《中国医院用药评价与分析》 2021年第7期820-825,共6页 Evaluation and Analysis of Drug-use in Hospitals of China
基金 河北省2020年度医学科学研究课题计划项目(No.20200194)。
关键词 胡黄连苷Ⅱ MEK/ERK通路 食管癌 侵袭转移 Picroside Ⅱ MEK/ERK pathway Esophageal cancer Invasion and metastasis
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