| 周香,王维明,郑志强,游涛.姜黄素联合FOLFOX诱导胃癌细胞发生凋亡及其机制研究[J].,2013,33(6):0810-0813 |
| 姜黄素联合FOLFOX诱导胃癌细胞发生凋亡及其机制研究 |
| Curcumin Combined FOLFOX Induced Cell Apoptosis of Gastric Cancer and Its Mechanism Research |
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| DOI：10.7661/CJIM.2013.06.0810 |
| 中文关键词: 姜黄素 5-氟尿嘧啶联合奥沙利铂化疗方案 胃癌 凋亡 |
| 英文关键词:curcumin FOLFOX gastric cancer apoptosis |
| 基金项目:温州市科技计划资助项目（No.Y20100033） |
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| 中文摘要: |
| 目的观察姜黄素联合FOLFOX（folinic acid fluorouracil oxaliplatin）对胃癌细胞株BGC-823生长的影响，并探讨其可能的发生机制。方法设立空白对照组、姜黄素组、FOLFOX组［5-FU（0.1 mmol/L）+奥沙利铂（5 μmol/L）］及姜黄素联合FOLFOX组。CCK8法检测细胞活性，Hoechst染色观察细胞凋亡，Caspase-3试剂盒检测Caspase-3活性， 实时荧光定量PCR法测定Bcl-2、Bax mRNA表达的变化，Western blot法测定Bcl-2、Bax蛋白表达的变化。结果各用药组均能抑制BGC-823细胞增殖、诱导细胞凋亡、增加Caspase-3的活性、降低Bcl-2 mRNA及Bcl-2蛋白表达而增加Bax mRNA及Bax蛋白表达，且姜黄素联合FOLFOX组疗效优于姜黄素组及FOLFOX组，差异有统计学意义（P<0.01）。结论姜黄素联合FOLFOX组能够明显抑制BGC-823细胞的增殖，其联合作用可能通过促进Bax的表达及Caspase-3的活性、抑制Bcl-2表达，从而加速肿瘤细胞的凋亡。 |
| 英文摘要: |
| ObjectiveTo observe the effect of curcumin combined folinic acid fluorouracil oxaliplatin （FOLFOX） on the gastric adenocarcinoma cell line BGC-823 and to explore its possible mechanisms. MethodsCells were divided into five groups， i.e. the blank control group， the curcumin group， the FOLFOX group （0.1 mmol/L 5-FU+5 μmol/L oxaliplatin）， and the curcumin combined FOLFOX group. CCK-8 was used to detect cell activity. The cell apoptosis was observed using Hoechst dyeing. Caspase-3 test kit was applied to test Caspase-3 vitality. The mRNA expressions of Bcl-2 and Bax were detected by real time fluorescent quantitative PCR. The expressions of Bcl-2 and Bax protein were determined by Western blot. ResultsThe BGC-823 cells′ proliferation could be inhibited， apoptosis induced， the Caspase-3 activity increased， expressions of Bcl-2 mRNA and Bcl-2 protein lowered， while Bax mRNA and Bax protein expressions increased in each medicated group. Besides， the efficacy of the curcumin combined FOLFOX group was superior to that of the curcumin group and the FOLFOX group， showing statistical difference （P<0.01）. ConclusionCurcumin combined FOLFOX could significantly inhibit the proliferation of BGC-823 cells possibly via promoting Bax expression and Caspase-3 activity， inhibiting Bcl-2 expression， thus inducing apoptosis. |
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