黄芪甲苷Ⅳ联合紫杉醇通过STAT3-NF-κB途径对胃癌细胞的作用研究

被引:15
作者
李全志 [1 ]
郑林静 [1 ]
刘志强 [2 ]
机构
[1] 河南省开封市肿瘤医院药剂科
[2] 河南大学附属淮河医院内科
关键词
胃癌; 黄芪甲苷Ⅳ; 紫杉醇; STAT3; NF-κB;
D O I
10.14053/j.cnki.ppcr.202201002
中图分类号
R735.2 [胃肿瘤];
学科分类号
100112 [医学生物化学与分子生物学];
摘要
目的探讨黄芪甲苷Ⅳ联合紫杉醇对胃癌细胞的作用及其可能的机制。方法黄芪甲苷Ⅳ和紫杉醇按给药剂量分为0μg/ml组、5μg/ml组、10μg/ml组、20μg/ml组、40μg/ml组、80μg/ml组和160μg/ml组处理胃癌细胞AGS。CCK-8试剂盒检测细胞活力;集落形成实验检测细胞增殖;流式细胞术检测细胞凋亡;Western blot检测Bax、Bcl-2和STAT3-NF-κB途径相关蛋白的表达;Transwell实验检测细胞迁移和侵袭。结果黄芪甲苷Ⅳ在20μg/ml、40μg/ml、80μg/ml和160μg/ml浓度下可明显抑制AGS细胞活力,黄芪甲苷Ⅳ IC50=63.99μg/ml;紫杉醇在10μg/ml、20μg/ml、40μg/ml、80μg/ml和160μg/ml浓度下可明显抑制AGS细胞活力,紫杉醇IC50=40.08μg/ml。与对照组相比,黄芪甲苷Ⅳ组、紫杉醇组和联合组的细胞活力、克隆形成数、细胞迁移和侵袭数明显降低(P<0.05),细胞凋亡率、Bax蛋白表达明显升高(P<0.05),Bcl-2、pSTAT3/STAT3和pNF-κB/NF-κB蛋白表达明显降低(P<0.05);与联合组比较,黄芪甲苷Ⅳ组和紫杉醇组的细胞活力、克隆形成数、细胞迁移和侵袭数明显升高(P<0.05),细胞凋亡率、Bax蛋白表达明显降低(P<0.05),Bcl-2、pSTAT3/STAT3和pNF-κB/NF-κB蛋白表达明显升高(P<0.05)。结论黄芪甲苷Ⅳ联合紫杉醇可抑制胃癌细胞增殖、迁移和侵袭,促进细胞凋亡,该作用可能是通过抑制STAT3-NF-κB途径实现的。
引用
收藏
页码:21 / 26
页数:6
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