摘要
目的:研究姜黄素联合索拉菲尼对肝癌细胞系HepG-2细胞增殖及自噬的影响。方法:体外培养肝癌细胞系HepG-2细胞,用不同浓度姜黄素(0、10、20、30、40、50 mmol/L)、不同浓度索拉菲尼(0、5、10、15、20μmol/L)及两药联合处理肝癌细胞系HepG-2细胞24 h后,用CCK8实验检测细胞存活率。用姜黄素30 mmol/L、索拉菲尼10μmol/L及两药联合处理肝癌细胞系HepG-2细胞24 h后,用荧光定量PCR检测自噬相关信号通路关键蛋白AKT、mTOR及自噬相关蛋白LC3-Ⅱ的mRNA表达情况。结果:姜黄素、索拉菲尼及两药联合对HepG-2细胞均有增殖抑制作用,且呈浓度依赖性。与姜黄素或索拉菲尼单药组相比,姜黄素联合索拉菲尼组能显著抑制肝癌细胞系HepG-2细胞的增殖(P<0.001);能显著抑制AKT、mTOR的mRNA表达而增加自噬相关蛋白LC3-Ⅱ的mRNA的表达(P<0.001)。结论:姜黄素联合索拉菲尼组抑制肝癌细胞系HepG-2细胞增殖作用较单药组明显增强,两药联合协同诱导肝癌细胞系HepG2细胞产生自噬,其作用机制可能与抑制PI3K/AKT/mTOR信号通路有关。
Objective： To study the effect of Curcumin, Sorafenib, Curcumin combined to proliferation and autophagyin in Vitro Hepatocellular Carcinoma HepG-2 Cells. Methods： HepG-2 cells were treated by different concentrations of Curcumin（0, 10, 20, 30, 40,50 mmol/L）, Sorafenib（0, 5, 10, 15, 20 μmol/L）alone and the combination（Curcumin 30 mmol/L combined with Sorafenib 10 μmol/L）for 24 h. Cell proliferation were detected by CCK8 assay. And the m RNA expression of autophagy-related protein AKT, mTOR and LC3 were detected by Real-time PCR. Results： Compared with using Curcumin or Sorafenib alone, the both combination group had more abilities to depressing the cell proliferation（P〈0.001）, decreasing the m RNA expression of autophagy-related protein AKT, mTOR and increasing that of LC3-Ⅱ（P〈0.001）. Conclusion： Curcumin combined with Sorafenib can effectively depress the cell proliferation in Vitro Hepatocellular Carcinoma HepG-2 Cells and maybe induce cell autophagy through PI3 K/AKT/m TOR signal pathway.
作者
刘国龄
沈方臻
孟令君
王耀庭
张炳远
LIU Guo-ling;SHEN Fang-zhen;MENG Ling-jun;WANG Yao-ting;ZHANG Bing-yuan(Department of Ontology,Affiliated Hospital of Qingdao University,Qingdao,Shandong,266003,China;Department of Hepatobiliary Surgery,Affiliated Hospital of Qingdao University,qingdao,Shandong,266003,China)
出处
《现代生物医学进展》
CAS
2018年第12期2268-2272,共5页
Progress in Modern Biomedicine
关键词
姜黄素
索拉菲尼
自噬
肝癌
Curcumin
Sorafenib
Autophagy
Hepatocellular Carcinoma
