防己诺林碱对胶质母细胞瘤抑制作用的实验研究
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- 论文作者：王迅 ; 吴文霄 ; 矫永庆 ; 崔鹏
- 年：2016
- 作者机构：大连市第三人民医院;大连医科大学附属第三临床学院神经外科;
- 论文关键词：防己诺林碱 ; 胶质母细胞瘤 ; U251细胞 ; AKT蛋白
- 英文论文关键词：Fangchinoline ; Glioblastoma cell ; U251 cells ; AKT protein
- 会议召开时间：2016-11-25
- 会议录名称：湖南中医药大学学报2016/专集：国际数字医学会数字中医药分会成立大会暨首届数字中医药学术交流会论文集
- 语种：中文
- 分类号：R96
- 学会代码：HNZY
- 会议名称：国际数字医学会数字中医药分会成立大会暨首届数字中医药学术交流会
- 会议地点：中国广东珠海
- 主办单位：国际数字医学会、Digital Chinese Medicine
- 学会名称：湖南中医药大学期刊杂志社
- 页数：2
- 文件大小：2250k
- 原文格式：D
- 会议级别：全国
摘要
目的探讨防己诺林碱对人胶质母细胞瘤U251细胞株的抑制作用及可能的机制。方法采用四甲基偶氮唑盐(MTT)比色法检测不同浓度防己诺林碱(FAN)处理U251细胞后的12h、24h及48h的细胞活力;通过划痕实验,检测不同浓度FAN对U251细胞迁移能力的影响;在分子机制研究中,运用免疫印迹(Western blot)方法检测经不同浓度FAN处理后,U251细胞中AKT蛋白质水平的变化。结果 FAN处理后12h、24h及48h明显抑制U251细胞增殖;用药48h后,FAN明显抑制U251细胞迁移,且具有浓度依赖性。用药48h,随着防己诺林碱浓度的升高,Thr308和Ser473位点磷酸化的AKT蛋白表达量而出现明显的下降趋势,但总的AKT蛋白表达量基本一致。结论 FAN能抑制U251细胞的增殖及迁移,其作用机制可能部分是通过钝化磷酸化的AKTp-Thr308和AKTp-Ser473,降低AKT活性来实现的。
Objective To investigate the inhibitory effect of fangchinoline on human glioblastoma cell line U251 and its possible mechanism. Methods Effect of cell viability using MTT assaywas used to detect different concentrations of fangchinoline treatment of U251 cells after 12 h, 24 h and 48h; by scratch test, detection of different concentrations of fan of U251 cells migration ability; inthe study of molecular mechanism of, using Western blot after treated with different concentration of fan, the level of AKT protein in U251 cells changes. Results After FAN treatment, 12 h, 24 h and 48 h obviously inhibited the proliferation of U251 cells. After treatment with 48 h, FAN significantly inhibited the migration of U251 cells, and had a concentration dependent. Medication for 48 h, with theincrease of fangchinoline concentration, thr308 and ser473 phosphorylation of Akt protein expression significantly decreased, but total AKT protein expression was equal to. Conclusions FAN caninhibit the proliferation and migration of U251 cells, and its mechanism may be partly through the inactivation of AKTp-Thr308 and AKTp-Ser473, which can decrease the activity of AKT.
Objective To investigate the inhibitory effect of fangchinoline on human glioblastoma cell line U251 and its possible mechanism. Methods Effect of cell viability using MTT assaywas used to detect different concentrations of fangchinoline treatment of U251 cells after 12 h, 24 h and 48h; by scratch test, detection of different concentrations of fan of U251 cells migration ability; inthe study of molecular mechanism of, using Western blot after treated with different concentration of fan, the level of AKT protein in U251 cells changes. Results After FAN treatment, 12 h, 24 h and 48 h obviously inhibited the proliferation of U251 cells. After treatment with 48 h, FAN significantly inhibited the migration of U251 cells, and had a concentration dependent. Medication for 48 h, with theincrease of fangchinoline concentration, thr308 and ser473 phosphorylation of Akt protein expression significantly decreased, but total AKT protein expression was equal to. Conclusions FAN caninhibit the proliferation and migration of U251 cells, and its mechanism may be partly through the inactivation of AKTp-Thr308 and AKTp-Ser473, which can decrease the activity of AKT.
引文
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[4]Wang C.D,Huang J.G,Gao X,et al.Fangchinoline induced Gl/S arrest bymodulating expression of p27,PCNA,and cyclin D in human prostate carcinoma cancer PC3 cells and tumor xenograft.J.Bioscience,biotechnology,and biochemistry.2010,74,488-93.
[5]Xing ZB,Yao L,Zhang GQ,et al.Fangchinoline inhibits breast adenocarcinoma proliferation by inducing apoptosis.J.Chemical&pharmaceutical bulletin 2011,59(12):1476-80.
[6]Wang N,Pan W,Zhu M,et al.Fangchinoline induces autophagic cell death viap 53/sestrin2/AMPK signalling in human hepatocellular carcinoma cells.J.British journal of pharmacology2011,164(2b):731-42.
[7]Wang Y,Chen J,Wang L,et al.Fangchinoline induces GO/Gl arrest by modulatingthe expression of CDKNl A and CCND2 in K562 human chronic myelogenous leukemia cells.J.Experimental and therapeutic medicine,2013,5,1105-12.
[8]Li X,Wu C,Chen N,Gu H,et al.PI3K/Akt/m TOR signaling pathway and targeted therapy for glioblastoma.J.Oncotarget.2016 Mar 7.