节点文献

灵芝酸B对乳腺癌细胞MCF-7增殖作用的影响

Effect of ganoderma acid B on proliferation of breast cancer cells MCF-7

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 李楠刘东璞姚海涛李子豪王抒张晓波

【Author】 LI Nan;LIU Dong-pu;YAO Hai-tao;LI Zi-hao;WANG Shu;ZHANG Xiao-bo;School of Basic Medicine, Jiamusi University;

【机构】 佳木斯大学基础医学院

【摘要】 目的:研究灵芝酸B在体外对人乳腺癌细胞MCF-7增殖的影响。方法:采用CCK8试剂盒分别检测对照组和不同浓度灵芝酸B (0、1、5、10、20、50、100μmol·L-1)对MCF-7细胞增殖的影响。每组设3个复孔,分别接种于96孔板中,分别于培养24h和48h检测其OD值。结果:CCK8法检测,与对照组相比,随着灵芝酸浓度增加,细胞存活率下降,当灵芝酸浓度为100μmol·L-1时,细胞存活率最低(P<0.05或P<0.01),细胞抑制作用最强。同时随着药物处理时间增长,细胞存活率下降。结论:表明灵芝酸的抑制作用具有浓度依赖性和时间依赖性。

【Abstract】 Objective: To study the effect of ganoderma acid B on McF-7 proliferation of human breast cancer cells in vitro.Methods: The study was divided into control group and B group with different concentration of ganoderma acid, including 0, 1, 5, 10, 20, 50 and 100 mol/L concentration group. The proliferation of McF-7 cells in each group was detected by CCK8 kit.Three compound Wells were set in each group and inoculated into 96-well plates, respectively. OD value was detected at 24 hours and 48 hours after culture.Results: Compared with the control group, the cell survival rate decreased with the increase of ganoderma acid concentration.When the concentration of ganoderma acid was 100 mol/L, the cell survival rate was the lowest(P<0.05 or P<0.01), and the cell inhibition was the strongest.At the same time, cell survival rate decreases with the increase of drug treatment time.The results showed that the inhibition of ganoderma acid was concentration-dependent and time-dependent.Conclusion: Ganoderma acid B can inhibit the proliferation of human breast cancer cells MCF-7, which may be a therapeutic agent for breast cancer.

【关键词】 灵芝酸BMCF-7细胞细胞增殖
【Key words】 ganoderma acid BMCF-7 cellcell proliferation
【基金】 省教育厅项目基本科研业务费人才培养项目,编号:2016-KYYWF-0111;佳木斯大学博士专项科研基金,编号:22Zb201508;黑龙江省大学生创新创业训练计划项目,编号:201910222091
  • 【文献出处】 黑龙江医药科学 ,Heilongjiang Medicine and Pharmacy , 编辑部邮箱 ,2019年04期
  • 【分类号】R285
  • 【被引频次】3
  • 【下载频次】236
节点文献中: 

本文链接的文献网络图示:

本文的引文网络