| 张 琼,余智操,博 伦,张红梅.阿帕替尼对人肝癌细胞增殖及凋亡的作用机制研究[J].,2019,19(13):2424-2428 |
| 阿帕替尼对人肝癌细胞增殖及凋亡的作用机制研究 |
| The Effect of Apatinib on The Proliferation and Apoptosis of Human Hepatocellular Carcinoma Cells |
| 投稿时间：2019-02-23 修订日期：2019-03-15 |
| DOI：10.13241/j.cnki.pmb.2019.13.005 |
| 中文关键词: 肝癌 阿帕替尼 细胞增殖 细胞凋亡 |
| 英文关键词: Hepatocellular carcinoma Apatinib Cell proliferation Apoptosis |
| 基金项目:国家自然科学基金面上项目(81572699)；陕西省重点产业创新链课题（2016KTZDSF-01-05） |
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| 中文摘要: |
| 摘要 目的：探讨阿帕替尼抑制肝癌细胞增殖促进凋亡的作用机制。方法：选取肝癌细胞系SNU739、HepG2，以CCK-8细胞增殖实验、平板克隆实验测定阿帕替尼对肝癌细胞增殖及克隆形成能力的影响；流式细胞术检测阿帕替尼对肝癌细胞凋亡的影响；蛋白免疫印迹法检测阿帕替尼影响肝癌细胞凋亡相关蛋白Bax、Bcl-2及Caspase3的表达情况。结果：与对照组相比，阿帕替尼可显著抑制肝癌细胞增殖（P<0.05）。平板克隆实验提示与对照组相比，10 μM和20 μM阿帕替尼组肝癌细胞克隆数明显减少（P<0.05）。流式细胞术结果提示10 μM和20 μM阿帕替尼处理组细胞凋亡率明显增加（P<0.05）。蛋白免疫印迹法结果显示经阿帕替尼处理的肝癌细胞，促凋亡蛋白Bax及Caspase3的活性片段Cleaved-caspase3表达水平显著上调，抗凋亡蛋白Bcl-2显著下调（P＜0.01）。结论：阿帕替尼通过调节肝癌细胞凋亡相关蛋白从而抑制肝癌细胞增殖、促进其凋亡。 |
| 英文摘要: |
| ABSTRACT Objective: The present study aimed to investigate the effects of Apatinib on the proliferation and apoptosis of human hepatocellular carcinoma cells. Methods: The proliferation and apoptosis of these hepatocellular carcinoma cells were assessed by CCK-8, plate cloning assay and flow cytometry, respectively. Finally, the levels of the apoptosis-associated proteins Bax, Bcl-2 and Caspase3 were detected by western blotting. Results: The proliferation of SNU739 and HepG2 cells were signifcantly inhibited by Apatinib, compared with the control group (P<0.05). The inhibitory effect of the Apatinib group was markedly stronger than that of the control group. Compared to the control group, the colony forming efficiency of hepatocellular carcinoma cells treated by 10 μM and 20 μM Apatinib were significantly lower (P<0.05), the rates of apoptosis were obviously higher (P<0.05). The expression levels of Bcl-2 was further inhibited in the Apatinib group, and the expression level of Bax and Cleaved-caspase3 werealso signifcantly increased in the Apatinib group by western blotting (P<0.01). Conclusion: Apatinib significantly inhibited the proliferation and promoted the apoptosis of hepatocellular carcinoma cells by upregulating the expression of Bax and Cleaved-caspase3, and downregulating the expression of Bcl-2. |
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