天津医药

天津医药 ›› 2015, Vol. 43 ›› Issue (11): 1267-1270.doi: 10.11958/j.issn.0253-9896.2015.11.012

• 细胞与分子生物学 • 上一篇    下一篇

异甘草素对胃癌 SGC7901 细胞侵袭能力的影响

刘方康， 牛琼， 王爱丽， 贾兴芳， 胡营滨， 刘成霞△#br#   

  1. 滨州医学院附属医院消化内科 （邮编 256603）
  • 收稿日期:2015-05-20 修回日期:2015-07-13 出版日期:2015-11-15 发布日期:2015-11-15
  • 通讯作者: 刘成霞 E-mail:phdlcx@163.com E-mail:993849195@qq.com
  • 作者简介:刘方康 （1988）， 男， 硕士在读， 主要从事消化道肿瘤研究

The impact of isoliquiritigenin on invasive ability of human gastric carcinoma SGC7901 cells

LIU Fangkang， NIU Qiong, WANG Aili, JIA Xingfang， HU Yingbin， LIU Chengxia△#br#   

  1. Department of Digestive Medicine, The Affiliated Hospital of Binzhou Medical University, Binzhou 256603, China
  • Received:2015-05-20 Revised:2015-07-13 Published:2015-11-15 Online:2015-11-15
  • Contact: LIU Chengxia E-mail:phdlcx@163.com E-mail:993849195@qq.com

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摘要： 目的 探讨异甘草素 （isoliquiritigenin） 对人胃癌 SGC7901 细胞侵袭能力的影响及其可能的分子机制。方法 取对数生长期人胃癌 SGC7901 细胞， 分为对照组（正常细胞培养液）， 异甘草素实验组(异甘草素溶于细胞培养液， 浓度分别为 10、 25、 50、 100 μmol/L)， 每组 4 个复孔。培养 24、 48、 72 h 后采用 MTT 法检测异甘草素对细胞生长的抑制情况， 摸索后续实验药物浓度和作用时间； 采用 Transwell 小室侵袭实验检测各组细胞的侵袭能力； Western blotting
法检测基质金属蛋白酶-9（MMP-9）、 蛋白激酶 B（Akt）和磷酸化 Akt（P-Akt）的表达。结果 10 μmol/L 异甘草素不能抑制胃癌细胞株 SGC7901 的生长， 而 25、 50、 100 μmol/L 异甘草素可明显抑制其生长， 且呈时间和浓度依赖性，24、 48、 72 h 半数抑制浓度（IC50）分别为 52.48、 44.49、 32.50 μmol/L， 故选定后续实验药物浓度为 25、 50、 100 μmol/L，作用时间为 24 h。与对照组穿膜细胞数（个： 209.75±9.29）相比， 25 μmol/L 组（138.50±10.15）、 50 μmol/L 组（89.50±16.56）、 100 μmol/L 组（45.00±8.08）逐渐降低（F=267.948， P < 0.05）。各组间 Akt 蛋白水平差异无统计学意义（F=1.492）； 随异甘草素浓度的增加， P-Akt、 MMP-9 蛋白水平逐渐降低（F 分别为 359.219、 431.324， 均 P < 0.05）。结论 异甘草素能够抑制 SGC7901 细胞侵袭能力， 其机制可能与下调 PI3K/Akt 信号转导通路蛋白及其下游的 MMP-9蛋白表达有关。

关键词: 异甘草素, 胃癌, 侵袭, PI3K/AKT, MMP9

Abstract: Objective To investigate the effects of isoliquiritigenin on the invasive ability of human gastric carcinoma SGC7901 cells, and its molecular mechanisms thereof. Methods The logarithmic phase human gastric carcinoma SGC7901 cells were divided into control group (normal cell culture fluid) and isoliquiritigenin group (isoliquiritigenin soluble in cell culture fluid, the concentrations were 10, 25, 50 and 100 μmol/L respectively). Each group had four repeated holes. The proliferation of SGC7901 cells were detected with MTT assay after 24 h, 48 h and 72 h of culture. The experimental drug concentration and action time were researched for the subsequent experiments. The in vitro invasion abilities of SGC7901 cells were assessed with Transwell test. The expression levels of MMP9, Akt and P-Akt were detected by Western blot assay. Results The proliferation of SGC7901 cells were inhibited by 10 μmol/L isoliquiritigenin, which can be significantly inhibited by 25, 50 and 100 μmol/L isoliquiritigenin in a concentration-dependent and time-dependent manner. The half inhibitory concentrations (IC50) of 24, 48 and 72 h were 52.48, 44.49 and 32.50 μmol/L, respectively. Therefore, the 25, 50 and 100 μmol/L isoliquiritigenin were selected as the subsequent experimental drug concentration, and 24 h was used as the action time. Compared with the control group (209.75±9.29), the membrane cell number of 25 μmol/L (138.50±10.15), 50 μmol/L (89.50±16.56) and 100 μmol/L (45.00±8.08) decreased gradually (F=267.948， P < 0.05). There was no significant difference in the expression level of Akt protein between four groups (F=1.492). The expression levels of P-Akt and MMP9 were gradually decreased with the increase of the isoliquirigenin concentration (F=359.219 and 431.324， P < 0.05). Conclusion Isoliquiritigenin can obviously inhibit invasion ability of SGC7901 cells, which may be related to the down regulation of the signal transduction pathway protein PI3K/Akt and the down steam protein MMP9.

Key words: glycyrrhiza uralensis, stomach neoplasms, matrix metalloproteinase 9, isoliquiritigenin,  invasive ability, PI3K/Akt, Akt,  P-Akt