| 甘草次酸选择性抑制肝癌细胞的增殖 |
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| 引用本文： | 张韫琪,蔡云,刘媛,赵博欣,李国锋. 甘草次酸选择性抑制肝癌细胞的增殖[J]. 南方医科大学学报, 2018, 38(4): 477 |
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| 作者姓名： | 张韫琪 蔡云 刘媛 赵博欣 李国锋 |
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| 摘 要： | 目的探讨甘草次酸对增殖速率不同的4株肝癌细胞SMMC-7721，SK-HEP1，HEPG2，HEP3B体外增殖的抑制作用及其机制。方法通过MTT法测定肝癌SMMC-7721，SK-HEP1，HEPG2和HEP3B细胞株体外生长曲线；用梯度浓度甘草次酸（5、10、20、30、40、60 μmol/L）分别刺激48 h后，MTT法检测甘草次酸对4种肝癌细胞株体外生长的影响，Western blot实验考察其对4种肝癌细胞株总ERK蛋白，磷酸化ERK蛋白和拓扑异构酶Ⅱα蛋白表达的影响。结果4株肝癌细胞中SMMC-7721细胞增殖速率最慢，而SK-HEP1 细胞增殖速率最快；甘草次酸刺激48 h 能浓度依赖性地抑制4 种肝癌细胞的生长，其中对慢增殖细胞SMMC-7721 细胞抑制作用最强（IC50为28.04 μmol/L）；细胞内ERK的磷酸化，拓扑异构酶Ⅱα的表达与细胞增殖速率呈正相关，SMMC-7721 细胞拓扑异构酶Ⅱα与p-ERK蛋白的表达在4 株细胞中最低，SK-HEP1 细胞表达最高。与阴性对照组相比，50 μmol/L的甘草次酸可显著抑制4株细胞内拓扑异构酶Ⅱα与p-ERK蛋白的表达（P<0.05），而25 μmol/L的甘草次酸可显著下调SMMC-7721，HEPG2和HEP3B细胞拓扑异构酶Ⅱα与p-ERK蛋白（P<0.05）而对SK-HEP1细胞没有作用。结论甘草次酸对不同肝癌细胞生长的抑制作用有选择性。其中对慢增殖肝癌的治疗具有较好的抑制效果。下调拓扑异构酶Ⅱα的表达与抑制ERK通路的激活可能为其作用机制之一。
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Glycyrrhetinic acid selectively inhibits proliferation of hepatocellular carcinoma cells invitro |
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| Abstract: | Objective To investigate the selective inhibitory effect of glycyrrhetinic acid on 4 hepatocellular carcinoma (HCC)cells with different proliferation rates and explore the underlying mechanisms. Methods MTT method was used to detect theproliferation rates of 4 HCC cell lines, namely SMMC-7721, SK-HEP1, HEPG2 and HEP3B. Following treatment of the cellswith glycyrrhetinic acid (5, 10, 20, 30, 40, and 60 μmol/L), the cell viability was analyzed using MTT assay and the expressionsof total ERK protein, p-ERK protein and topoisomerase IIα were detected using Western blotting. Results Among the 4 celllines, SMMC-7721 had the lowest and SK-HEP1 had the highest proliferation rate. Treatment with glycyrrhetinic acid for 48 hdose-dependently inhibited the proliferation of all the 4 cell lines in vitro and produced the strongest inhibitory effect inSMMC-7721 cells with the IC50 of 28.04 μmol/L. The proliferation rate of the cells was positively correlated with the expressionlevels of p-ERK and topoisomerase IIα, which were the lowest in SMMC-7721 cells and the highest in SK-HEP1 cells.Treatment with 50 μmol/L glycyrrhetinic acid significantly down-regulated the expressions of p-ERK and topoisomerase IIα inthe 4 HCC cell lines (P<0.05), while 25 μmol/L glycyrrhetinic acid significantly reduced the expression of topoisomerase IIαand p-ERK in SMMC-7721, HEPG2 and HEP3B cells (P<0.05) but not in SK-HEP1 cells. Conclusion Glycyrrhetinic acid caninhibit the proliferation of different HCC cells particularly in cells with a low proliferation rate. The inhibitory effect ofglycyrrhetinic acid might be mediated by reducing the expressions of topoisomerase IIα and inhibiting the ERK pathway. |
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