| 赵东晓,陈弘磊,孟冠敏,李芳琼,王伟.低浓度雷公藤甲素联合顺铂对肝癌细胞HepG2活性的影响[J].浙江中西医结合杂志,2017,27(5): |
| 低浓度雷公藤甲素联合顺铂对肝癌细胞HepG2活性的影响 |
| Effect of Low Concentration of Triptolide combined with Cisplatin on the activity of Liver Cancer HepG2 Cells |
| 投稿时间：2016-08-30 修订日期：2016-12-12 |
| DOI： |
| 中文关键词: 雷公藤甲素 顺铂 肝癌细胞 耐药 P糖蛋白 |
| 英文关键词:Triptolide Cisplatin Liver cancer cell Drug resistance P-glycoprotein |
| 基金项目:浙江省科技条件建设项目（No.2014F10014） |
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| 中文摘要: |
| 目的：探讨低浓度的雷公藤甲素与顺铂联合用药对人肝癌细胞HepG2活性的影响，及其逆转顺铂耐药的可能机制。方法：将人肝癌细胞HepG2分为顺铂单用组和雷公藤甲素与顺铂联用组。顺铂单用组用浓度为2.5、5、10、20、40 μg/ml的顺铂处理，联用组用顺铂（2.5、5、10、20、40 μg/ml）分别联合低浓度的雷公藤甲素（12.5 ng/ml）处理HepG2。CCK-8法检测HepG2细胞增殖的抑制率；流式细胞术检测细胞凋亡率和细胞内P糖蛋白的表达。结果：CCK-8结果表明，顺铂单独用药时(0、5、10、40 μg/mL)对肝癌细胞HepG2的细胞活力的抑制率分别为0、(4.0±1.0)%、(9.7±1.1)%、(29.4±2.4)%、(47.5±2.5)%、(62.9±1.2)%，而两者联合用药后抑制率分别增加为(4.7±1.0)%、(37.1±3.1)%、(44.1±3.5)%、(57.9±3.0)%、(66.9±2.0)%、(74.9±2.0)%，两组间对比细胞活力抑制率差异有统计学意义（P<0.01），且两药联合具有协同作用（P<0.01）；Annexin V/PI双染法检测细胞凋亡后发现，顺铂单用组诱导HepG2肝癌细胞凋亡率分别为 (4.3±0.3)%、(8.4±0.3)%、(9.6±0.3)%、(32.3±2.0)%，而联合用药组细胞凋亡率明显增加为 (9.6±0.4)%、(16.2±0.2)%、(23.2±0.5)%、53.0±3.6%)，两组间对比细胞凋亡率差异有统计学意义（P<0.01）；PE单染检测P糖蛋白后发现，顺铂单用后细胞内P糖蛋白表达率为(37.3±0.4)%、(34.2±0.5)%、(30.1±1.1)%、(34.2±2.3)%，无明显变化，而联合雷公藤甲素用药后P糖蛋白的表达率显著降低为(25.0±1.8)%、(18.6±0.7)%、(8.9±0.3)%、(1.8±0.1)%，两组间P糖蛋白表达差异有统计学意义（P<0.01）。结论：雷公藤甲素与顺铂联合用药可以显著抑制人肝癌HepG2的增殖并诱导凋亡，同时调节HepG2的顺铂耐药性，其作用机制可能与P糖蛋白下调相关，从而对肝癌细胞HepG2发挥抗肿瘤作用。 |
| 英文摘要: |
| Abstract: Objective: To investigate the synergistic effect of combination regimens of triptolide and Cisplatin and to explore its chemo-resistance reversal mechanism in human liver cancer cell line HepG2. Methods: The HepG2 cells were divided to two groups: Cisplatin group (2.5, 5, 10, 20, 40 μg/ml) and triptolide (12.5ng/ml) combined Cisplatin group. The CCK-8 test was used to estimate the inhibition of cell proliferation．Flow cytometry was applied to analyze the cell apoptosis and the expression of P-glycoprotein．Results: Compared with the single Cisplatin treated group, triptolide combined with Cisplatin depressed the proliferation of HepG2 cells significantly. Cell viability inhibitory rate of HepG2 cells in Cisplatin group were 0, (4.0±1.0)%, (9.7±1.1)%, (29.4±2.4)%, (47.5±2.5)%, (62.9±1.2)%, combination therapy increased the inhibition rate to (4.7±1.0)%, (37.1±3.1)%, (44.1±3.5)%, (57.9±3.0)%, (66.9±2.0)%, (74.9±2.0)%, with a significant difference among them (P <0.01). Besides, triptolide combined with Different doses of Cisplatin (0, 5, 10, 40μg/mL) significantly induced cell apoptosis in HepG2. The rate of cell apoptosis was increased from (4.3±0.3)%, (8.4±0.3)%, (9.6±0.3)%, (32.3±2.0)% to (9.6±0.4)%, (16.2±0.2)%, (23.2±0.5)%, 53.0±3.6%), respectively, with a significant difference among them (P <0.01); After combined use of the triptolide, rates of change of the expression of P-glycoprotein were decreased compared to that of single Cisplatin group, varying from (37.3±0.4)%, (34.2±0.5)%, (30.1±1.1)%, (34.2±2.3)% to (25.0±1.8)%, (18.6±0.7)%, (8.9±0.3)%, (1.8±0.1)%, with a significant difference among groups (P<0.01). Conclusion: triptolide combined with Cisplatin could substantially suppress proliferation, induce apoptosis on HepG2 cells and modulated cisplatin resistance of the human liver cancer cell line HepG2, the mechanism maybe related to the decrease of P-glycoprotein expression. |
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