| 关 波,张 松,郭 舜,石 磊,戚志华,李诗草,刘琳娜.大黄素抑制胃癌细胞糖酵解并促进凋亡[J].,2018,(13):2437-2441 |
| 大黄素抑制胃癌细胞糖酵解并促进凋亡 |
| Emodin Inhibits Glycolysis and Promotes Apoptosis of Gastric Cancer Cells |
| 投稿时间：2018-01-25 修订日期：2018-03-01 |
| DOI：10.13241/j.cnki.pmb.2018.13.007 |
| 中文关键词: 大黄素 己糖激酶Ⅱ 胃癌细胞 凋亡 |
| 英文关键词: Emodin Hexokinase II Gastric cancer cells Apoptosis |
| 基金项目:陕西省重点研究发展计划项目（2017SF-136）；陕西省中医药管理局中医药科研项目(ZYMS008) |
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| 中文摘要: |
| 摘要 目的：探讨大黄素对人胃癌BGC-823细胞凋亡及糖酵解的影响。方法：采用不同浓度大黄素(30 μmol /L、90 μmol /L、180 μmol /L)、磷脂酰肌醇3-激酶(Phosphatidylinositol 3 kinase，PI3K)抑制剂处理人胃癌BGC-823细胞，通过四甲基偶氮唑盐(MTT)检测细胞活力，采用试剂盒检测细胞葡萄糖消耗及乳酸水平，western blotting检测细胞己糖激酶Ⅱ、Bcl-2相关蛋白(Bcl-2 Associated X Protein, Bax)、PI3K、人低氧诱导因子1α (Human Hypoxia-inducible factor 1α,HIF-α)的表达。结果：大黄素能浓度依赖性的抑制BGC-823 细胞增殖、葡萄糖消耗，降低乳酸水平；并降低己糖激酶Ⅱ的表达，促进凋亡蛋白Bax表达。PI3K抑制剂可抑制胃癌细胞糖酵解水平，而将大黄素与PI3K抑制剂联合使用后，与单一抑制剂组比，对细胞糖酵解抑制水平进一步加强，大黄素可下调PI3K下游蛋白及HIF-α的表达。结论：大黄素对人胃癌BGC-823细胞的增殖抑制作用其作用机制与调节PI3K途径及HIF-α，并抑制己糖激酶Ⅱ表达降低胃癌细胞糖酵解水平相关。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effects of emodin on human gastric cancer BGC-823 cell apoptosis and glycolysis. Methods: Using different concentrations of emodin (30 mol/L, 90 mol/L, 180 mol/L), phosphatidylinositol 3- kinase (Phosphatidylinositol 3 kinase, PI3K) inhibitor treatment of human gastric cancer cell line BGC-823, cell vitality was detected by four methyl thiazolyl tetrazolium (MTT) assay kit, glucose consumption and lactate level in gastric cancer cells were also detected, the effect of emodin on human gastric cancer cells hexokinase II and Bcl-2 Associated X Protein(Bax), PI3K, Human Hypoxia-inducible factor 1α(HIF-α) were determinated. The effect of emodin on glycolysis of human gastric cancer BGC-823 cells was investigated by PI3K inhibitors. Results: Emodin inhibited human gastric cancer BGC-823 cell growth in concentration dependent manner, also significantly decreased glucose consumption and lactate levels; inhibited gastric cancer cell hexose kinase II expression, while promoting the regulation of apoptosis protein Bax expression. PI3K inhibitors also can inhibit the gastric cancer cell glycolysis level. The combination of emodin and PI3K inhibitor enhanced the glycolytic inhibition level of cells compared with the single inhibitor group. Emodin also reduced the expression of downstream of PI3K protein and HIF-α. Conclusion: Emodin has a significant inhibitory effect on the proliferation of human gastric cancer BGC-823 cells, and its mechanism may be related to its regulation of downstream of PI3K protein and HIF-α, thereby inhibiting the expression of hexokinase II and decreasing the glycolytic level of gastric cancer cells. |
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