| 刘国龄,沈方臻,孟令君,王耀庭,张炳远.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[J].,2018,(12):2268-2272 |
| 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 |
| Effect of Curcumin Combined with Sorafenib to Proliferation and Autophagy in Vitro Hepatocellular Carcinoma HepG-2 Cells |
| 投稿时间：2017-12-28 修订日期：2018-01-25 |
| DOI：10.13241/j.cnki.pmb.2018.12.014 |
| 中文关键词: 姜黄素 索拉菲尼 自噬 肝癌 |
| 英文关键词: Curcumin Sorafenib Autophagy Hepatocellular Carcinoma |
| 基金项目: |
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| 摘要点击次数: 348 |
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| 中文摘要: |
| 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、20 μmol/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10 μmol/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。 |
| 英文摘要: |
| ABSTRACT 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 30mmol/L combined with Sorafenib 10 μmol/L）for 24 h. Cell proliferation were detected by CCK8 assay. And the mRNA 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 abil- ities to depressing the cell proliferation (P<0.001), decreasing the mRNA expression of autophagy-related protein AKT, mTOR and in- creasing 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 PI3K/AKT/ mTOR signal pathway. |
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