上海交通大学学报（医学版）

›› 2011, Vol. 31 ›› Issue (7): 922-.doi: 10.3969/j.issn.1674-8115.2011.07.012

• 论著（基础研究） • 上一篇    下一篇

北冬虫夏草水提物对人肺腺癌细胞A549的作用

颜晶晶1, 唐永范2, 陆魏杰2, 张 鑫2, 孙加源1, 韩宝惠1   

  1. 1.上海交通大学附属胸科医院肺内科, 上海 200030； 2.上海国宝企业发展中心, 上海 200001
  • 出版日期:2011-07-28 发布日期:2011-07-27
  • 通讯作者: 韩宝惠, 电子信箱: xkyyhan@gmail.com；孙加源, 电子信箱: jysun1976@yahoo.com.cn。
  • 作者简介:颜晶晶（1985—）, 女, 硕士生；电子信箱: yanjing850103@163.com。
  • 基金资助:

    国家高技术研究发展计划（“863”计划）（2007AA021502）和上海市人才发展基金(2008044)

Effects of Cordyceps militaris extract on human pulmonary adenocarcinoma cell line A549

YAN Jing-jing1, TANG Yong-fan2, LU Wei-jie2, ZHANG Xin2, SUN Jia-yuan1, HAN Bao-hui1   

  1. 1.Department of Pulmonary Medicine, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, China；2.Shanghai Guobao Enterprise Development Center, Shanghai 200001, China
  • Online:2011-07-28 Published:2011-07-27
  • Supported by:

    National High-tech Research and Development Program of China, “863” Program, 2007AA021502；Shanghai Talent Development Fund, 2008044

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摘要：

目的 探讨北冬虫夏草水提物（CME）对人肺腺癌细胞A549的作用。方法 以不同质量浓度的CME处理A549细胞24、48、72 h，CCK8 法检测细胞生长抑制率。以0.5 mg/mL CME处理A549细胞（干预组）12、24和48 h，流式细胞术检测细胞周期和细胞凋亡率，Western blotting检测A549细胞增殖相关蛋白（p-ERK和p-Akt）和凋亡相关蛋白（caspase-3）的表达；以未予CME处理的A549细胞作为对照组。结果 A549细胞生长抑制率随CME质量浓度的升高和处理时间的延长而上升，呈明显的浓度-时间依赖性（P<0.01）。与对照组比较，干预组G2/M期细胞比例明显增加（P<0.01）；干预组细胞凋亡率显著高于对照组（P<0.01），且与CME处理时间呈显著正相关（r=0.995，P<0.01）；干预组p-ERK和p-Akt表达明显低于对照组，且与CME处理时间呈显著负相关（r=－0.881，P<0.01；r=－0.932，P<0.01）；干预组caspase-3表达显著高于对照组（P<0.05），且与CME处理时间呈显著正相关（r=0.681，P<0.01）。结论 CME对A549细胞生长的抑制作用可能与其使细胞阻滞于G2/M期并诱导细胞凋亡有关；CME有望成为肺腺癌辅助治疗药物。

关键词: 北冬虫夏草水提物, 肺腺癌, 细胞凋亡, 细胞周期阻滞

Abstract:

Objective To investigate the effects of Cordyceps militaris extract (CME) on human pulmonary adenocarcinoma cell line A549. Methods A549 cells were treated with CME of different mass concentrations for 24 h, 48 h and 72 h, and the inhibition rates of A549 cell proliferation were measured by CCK8 assay. A549 cells were treated with 0.5 mg/mL of CME (treatment group) for 12 h, 24 h and 48 h, cell cycle and cell apoptosis rates were determined by flow cytometry, and the expression of proliferation-related proteins (p-ERK and p-Akt) and apoptosis related protein (caspase-3) of A549 cells was determined by Western blotting. A549 cells without treatment with CME were served as control group. Results The inhibition rates of A549 cell proliferation increased with the mass concentrations of CME and time of treatment with CME, exhibiting a significant dose- and time-dependent manner (P<0.01). The percent of cells in G2/M phase in treatment group was significantly higher than that in control group (P<0.01). The cell apoptosis rates in treatment group were significantly higher than those in control group (P<0.01), and were significantly positively related to time of treatment with CME (r=0.995, P<0.01). The expression of p-ERK and p-Akt in treatment group was significantly lower than that in control group, and were significantly negatively related to time of treatment with CME (r=－0.881，P<0.01；r=－0.932，P<0.01). The expression of caspase-3 in treatment group was significantly higher than that in control group (P<0.05), and were significantly positively related to time of treatment with CME (r=0.681, P<0.01). Conclusion CEM can inhibit proliferation of A549 cells by inducing cell apoptosis and G2/M arrest, which may be used in the adjuvant therapy for pulmonary adenocarcinoma.

Key words: Cordyceps militaris extract, pulmonary adenocarcinoma, cell apoptosis, cell cycle arrest