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中国临床药理学与治疗学 ›› 2012, Vol. 17 ›› Issue (1): 1-5.

• 基础研究 •    下一篇

脂氧合酶抑制剂对肝癌细胞株HepG2增殖及MEK/ERK信号通路的影响

熊奇如1, 夏俊1, 李立祥2, 钱叶本1, 余宏铸1, 许业传1   

  1. 1安徽医科大学第一附属医院普外科,合肥 230022,安徽;
    2庐江县人民医院普外科,庐江 231500,安徽
  • 收稿日期:2011-08-23 修回日期:2011-11-02 出版日期:2012-01-26 发布日期:2012-02-16
  • 作者简介:熊奇如,男,博士,主任医师,长期从事肝癌基础与临床研究。E-mail: jun3jun2xia1@163.com
  • 基金资助:
    安徽省自然科学基金项目(090413144)

Effects of lipoxygenase inhibitor on proliferation of HepG2 cell line and MEK/ERK signaling pathway

XIONG Qi-ru1, XIA Jun1, LI Li-xiang2, QIAN Ye-ben1, YU Hong-zhu1, XU Ye-chuan1   

  1. 1Department of Hepatobiliary Surgery, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui, China;
    2Department of Surgery, Country People's Hospital of Lujiang, Lujiang 231500, Anhui, China
  • Received:2011-08-23 Revised:2011-11-02 Online:2012-01-26 Published:2012-02-16

摘要: 目的: 探讨脂氧合酶抑制剂去甲二氢愈创木酸(NDGA)对肝癌细胞株HepG2增殖及MEK/ERK信号通路的影响。方法: 在不同浓度的NDGA干预下对HepG2细胞进行体外培养;应用MTT比色法观察NDGA对HepG2增殖的影响;逆转录PCR(RT-PCR)测定不同浓度NDGA干预下丝裂原活化蛋白激酶的激酶(MEK)1、MEK2、细胞外信号调节激酶(ERK)1、ERK2 mRNA表达强度。结果: NDGA可抑制HepG2细胞增殖,且呈剂量依赖性;NDGA干预后HepG2细胞中MEK1、MEK2、ERK1、ERK2 mRNA的表达强度随着浓度的增加呈递减趋势;不同浓度NDGA干预均显著降低MEK1 mRNA的表达强度(P<0.05),在NDGA干预浓度为 100 μmol/L 及 200 μmol/L 时可显著降低MEK2、ERK1、ERK2 mRNA表达强度(P<0.05)。结论: NDGA可抑制HepG2细胞增殖,其作用机制与抑制MEK/ERK信号通路有关。

关键词: 脂氧合酶抑制剂, 肝癌, 细胞增殖, 细胞外信号调节激酶

Abstract: AIM: To investigate the effects of lipoxygenase inhibitor, on proliferation in hepatocellular carcinoma cell line HepG2 and MEK/ERK signaling pathway in vitro.METHODS: Different concentrations of nordihydroguaiaretic acid (NDGA) were used to treat HepG2 cell. The proliferation inhibition was analysed by alive cell count, MTT assay, the mRNA expression intensity of MEK1, MEK2, ERK1, ERK2 were examined by RT-PCR.RESULTS: NDGA can inhibit HepG2 cell proliferation viability in the dose-dependent manner. The mRNA expression intensity of MEK1, MEK2, ERK1, ERK2 showed a trend of decreasing while the concentrations of nordihydroguaiaretic acid increased. The mRNA expression intensity of MEK1 was significantly decreased than the control at any concentrations (P<0.05), meanwhile the mRNA expression intensity of MEK2, ERK1, ERK2 was significantly decreased than the control at concentrations of 100 μmol/L or 200 μmol/L (P<0.05).CONCLUSION: NDGA can inhibit proliferation of HepG2 cell line, the mechanism of which may be due to down-regulating MEK/ERK signaling pathway.

Key words: Lipoxygenase inhibitors, Hepatocellular carcinoma, Cell proliferation, Extracellular signal-regulated kinase

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