姜黄素联合LY294002对鼠卵巢癌转基因细胞系T1、T2、T3的抑制作用  被引量:3

Inhibitory effects of curcumin with LY294002 on the proliferation of mouse transgenic ovarian cancer cell lines T1,T2 and T3

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作  者:曹程程[1] 夏光[1] 高英卓[1] 吕庆杰[1] CAO Cheng-cheng;XIA Guang;GAO Ying-zhuo;L Qing-jie(Department of Pathology,Shengjing Hospital of China Medical University,Shenyang 110004,China)

机构地区:[1]中国医科大学附属盛京医院病理科,沈阳110004

出  处:《临床与实验病理学杂志》2018年第9期978-982,共5页Chinese Journal of Clinical and Experimental Pathology

基  金:辽宁省"百千万人才工程"资助项目(2011921040);辽宁省科技攻关计划项目(2013225021);沈阳市科技创新专项资金-应用基础研究专项(F14-231-1-46)

摘  要:目的探讨姜黄素与PI3K抑制剂LY294002及两者联合用药对鼠卵巢癌转基因细胞系T1、T2、T3的增殖抑制作用及其作用机制。方法体外培养鼠卵巢癌转基因细胞系T1、T2、T3,0~80μmol/L姜黄素与相同浓度LY294002单独及联合用药分别作用12、24、48 h,MTT方法检测T1、T2、T3细胞的增殖活性;Western blot法检测细胞内Akt、p-Akt蛋白表达水平。结果姜黄素能显著抑制T1、T2、T3细胞增殖,呈时间与剂量依赖性,其中对T2、T3抑制作用更明显;姜黄素明显降低T2、T3细胞内p-Akt蛋白的表达,对Akt蛋白表达改变不明显;姜黄素与LY294002联合用药明显加强姜黄素对T2、T3细胞增殖抑制作用。结论姜黄素能显著抑制Akt转基因型细胞系T2和T3的生长;小剂量PI3K抑制剂LY294002即能明显增强其对Akt转基因型细胞系T2、T3的增殖抑制作用,其作用机制可能是通过PI3K/Akt通路下调p-Akt表达来实现的。To study the suppressive effect and its mechanisms of curcumin and LY294002,an inhibitor of PI3K/Akt signal pathway,and their combination on growth and proliferation of transgenic ovarian cancer cell lines T1,T2 and T3.Methods The cell lines were treated with 0~80μmol/L curcumin,LY294002 and their combination for 12 h,24 h and 48 h,and MTT essay was used to examine the suppressive effect of curcumin on the proliferation.Western blot assay was used to determine the Akt and p-Akt protien levels of expression.Results Curcumin inhibited the proliferation of T1,T2 and T3 cells in a time and dose-dependent manner,and the effects were stronger on T2 and T3 cells.Curcumin obviously down regulated the expression of p-Akt,while nothing with Akt in T2 and T3 cells.The combination of curcumin and LY294002 obviously strengthened the inhibitory effect of T2 and T3 cells.Conclusion Curcumin can suppress the proliferation of cell lines T2 and T3 with Akt transgenic type obviously,and low dosage of LY294002 can strengthen the inhibitory effects on T2 and T3 cells.The mechanism may be that down-regulate the expression of p-Akt via PI3K/Akt signal pathway.

关 键 词:卵巢肿瘤 姜黄素 LY294002 P-AKT PI3K/Akt 

分 类 号:R730.2[医药卫生—肿瘤]

 

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