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  

Effect of astragaloside Ⅳ combined with paclitaxel on gastric cancer cells through STAT3-NF-κB pathway

作　　者：李全志 郑林静 刘志强[2] LI Quan-zhi;ZHENG Lin-jing;LIU Zhi-qiang(Department of Pharmacy,Kaifeng Tumor Hospital,Kaifeng 475000,China;Department of Internal Medicine,Huaihe Hospital Affiliated to Henan University,Kaifeng 475000,China)

机构地区：[1]河南省开封市肿瘤医院药剂科,河南开封475000 [2]河南大学附属淮河医院内科,河南开封475000

出　　处：《实用药物与临床》2022年第1期21-26,共6页Practical Pharmacy and Clinical Remedies

基　　金：河南省科技计划发展项目(202102110023)。

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 IC_(50)=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IC_(50)=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。Objective To investigate the effect of astragaloside Ⅳ combined with paclitaxel on gastric cancer cells and its possible mechanism.Methods Astragaloside Ⅳ and paclitaxel were used to treat gastric cancer cell AGS with concentration of 0 μg/ml, 5 μg/ml, 10 μg/ml, 20 μg/ml, 40 μg/ml, 80 μg/ml and 160 μg/ml, CCK-8 kit was used to detect cell viability;colony formation test was used to detect cell proliferation;flow cytometry was used to detect cell apoptosis;Western blot was used to detect the expression of proteins related to Bax, Bcl-2 and STAT3-NF-κB pathway;Transwell experiment was used to detect cell migration and invasion.Results Astragaloside Ⅳ could significantly inhibit the viability of AGS cells at the concentrations of 20 μg/ml, 40 μg/ml, 80 μg/ml and 160 μg/ml.The IC_(50) of astragaloside Ⅳ was 63.99 μg/ml;Paclitaxel could significantly inhibit the viability of AGS cells at the concentration of 10 μg/ml, 20 μg/ml, 40 μg/ml, 80 μg/ml and 160 μg/ml.The IC_(50) of paclitaxel was 40.08 μg/ml.Compared with the control group, the cell viability, colony formation number, cell migration and invasion number of the astragaloside Ⅳ group, paclitaxel group and the combination group were significantly decreased(P<0.05),and the apoptosis rate and Bax protein expression were significantly increased(P<0.05),while Bcl-2,pSTAT3/STAT3 and pNF-κB/NF-κB protein expression was significantly decreased(P<0.05);compared with the combination group, cell viability, colony formation number and the number of cell migration and invasion in astragaloside Ⅳ and paclitaxel groups were significantly increased(P<0.05),the rate of apoptosis and Bax protein expression were significantly decreased(P<0.05),while the expression of Bcl-2,pSTAT3/STAT3 and pNF-κB/NF-κB protein was significantly increased(P<0.05).Conclusion Astragaloside Ⅳ combined with paclitaxel can inhibit the proliferation, migration and invasion of gastric cancer cells, and promote cell apoptosis, which may be achieved by inhibiting the ST

关 键 词：胃癌 黄芪甲苷Ⅳ 紫杉醇 STAT3 NF-ΚB 

分 类 号：R735.2[医药卫生—肿瘤]