布洛芬抑制人肝癌细胞BEL-7402生长及机制的初步研究

张婷; 吴惠毅; 张欢欢

doi:10.3969/j.issn.1007-3969.2015.04.009

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布洛芬抑制人肝癌细胞BEL-7402生长及机制的初步研究

更新时间：2025-12-31

- 布洛芬抑制人肝癌细胞BEL-7402生长及机制的初步研究
- The inhibition of ibuprofen on the growth of hepatoma carcinoma cell BEL-7402 and the preliminary mechanisms
- 中国癌症杂志 2015年25卷第4期页码：294-299
- 作者机构：
  
  连云港市第一人民医院中心实验室,江苏,连云港,222002
- 作者简介：
- 基金信息：
  
  连云港市科技计划项目(SH1219)。
- DOI：10.3969/j.issn.1007-3969.2015.04.009
  中图分类号：
- 网络出版：2015-05-25，
  
  纸质出版：2015-05-25
- 稿件说明：
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张婷,吴惠毅,张欢欢,等. 布洛芬抑制人肝癌细胞BEL-7402生长及机制的初步研究[J]. 中国癌症杂志, 2015, 25(4): 294-299.

张婷, 吴惠毅, 张欢欢. The inhibition of ibuprofen on the growth of hepatoma carcinoma cell BEL-7402 and the preliminary mechanisms[J]. China Oncology, 2015, 25(4): 294-299.
张婷,吴惠毅,张欢欢,等. 布洛芬抑制人肝癌细胞BEL-7402生长及机制的初步研究[J]. 中国癌症杂志, 2015, 25(4): 294-299. DOI： 10.3969/j.issn.1007-3969.2015.04.009.

张婷, 吴惠毅, 张欢欢. The inhibition of ibuprofen on the growth of hepatoma carcinoma cell BEL-7402 and the preliminary mechanisms[J]. China Oncology, 2015, 25(4): 294-299. DOI： 10.3969/j.issn.1007-3969.2015.04.009.

摘要

背景与目的：近来发现，临床上常用的非甾体类抗炎药(non-steroidal anti-inflammatory drugs，NSAIDs)可以降低多种癌症的发病率。布洛芬(ibuprofen)作为一种常用的NSAIDs，对肝癌是否具有抑制作用，国内外鲜有报道。本研究初步探讨布洛芬抑制肝癌细胞BEL-7402的作用，并研究其相关机制。方法：肝癌细胞BEL-7402分为对照组和不同浓度布洛芬处理组，药物处理0、24、48和72 h后用MTT法检测各组细胞增殖抑制率；流式细胞术检测各组细胞的周期分布；细胞分析仪检测各组细胞活力及细胞凋亡；蛋白[质

]

印迹(Western blot)检测各组细胞增殖性核抗原(PCNA)、细胞周期蛋白(Cyclin D1)、B细胞淋巴瘤/白血病-2 (Bcl-2)和环氧合酶-2(COX-2)蛋白的表达；ELISA法检测细胞培养上清液中前列腺素E

(PGE

)蛋白表达水平。结果：布洛芬组中BEL-7402细胞增殖受到抑制，且抑制作用呈时间和剂量依赖性(P0.05)。2.0 mmol/L布洛芬组48 h细胞活力明显低于对照组［(47.87±5.23)% vs (88.93±5.49)%］，G

期细胞比例明显高于对照组［(80.04±3.61)%vs (62.36±8.33)%］，细胞早期凋亡率明显高于对照组［(36.65±10.07)% vs (9.81±6.80)%］，差异有统计学意义(P0.05)。布洛芬作用于细胞48 h后，PCNA、Cyclin D1、Bcl-2以及COX-2蛋白表达与对照组相比显著减少(P0.05)；细胞培养上清液中PGE

蛋白表达量与对照组［(23.98±4.89) ng/L vs (68.70±9.43) ng/L］相比，显著降低(P0.01)。结论：布洛芬能够抑制肝癌细胞BEL-7402增殖与活力，阻滞细胞周期，促进细胞凋亡，其作用机制可能与抑制COX-2及PGE

表达有关。

Abstract

Background and purpose: Recently

studies showed that non-steroidal anti-inflammatory drugs (NSAIDs) could reduce the incidence of cancer. Whether ibuprofen could inhibit the growth of hepatocellular carcinoma cells had not been reported yet. In the current study

we investigated the effects of ibuprof

en on hepatoma carcinoma BEL-7402 cells and the relevant mechanisms. Methods: Hepatocellular carcinoma BEL-7402 cells were randomly divided into 7 groups: the control group and the ibuprofen groups (0.1

0.5

1.0

2.0

3.0 and 4.0 mmol/L). The effect of ibuprofen on BEL-7402 HCC cells was measured by MTT method

the cell cycles were analyzed by flow cytometry (FCM)

cell vitality and apoptosis were determined by cell analyzer. PCNA

Cyclin D1

Bcl-2 and COX-2 protein levels were examined by Western blot

and the expressions of prostaglandin E

(PGE

) were measured by ELISA. Results: After the exposure to ibuprofen

the suppression ratio of BEL-7402 cells was increased (P0.05). BEL-7402 cell vitality was decreased by degrees significantly (P0.05)

early apoptosis of BEL-7402 cells was increased (P0.05)

and the G

phase ratio was increased significantly compared with control group (P0.05). Ibuprofen effectively decreased PCNA

Cyclin D1

Bcl-2 and COX-2 expressions in BEL-7402 cells (P0.05)

and decreased PGE

protein expression in cell culture supernatants significantly (P0.05). Conclusion: Ibuprofen is effective for inhibiting the proliferations

increasing apoptosis and blocking cell cycles of BEL-7402 HCC cells. The anti-tumor mechanisms of ibuprofen may be related with the inhibition of COX-2 and PGE

expressions.

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