青藤碱与卡铂对宫颈癌Hela细胞增殖的协同抑制研究

The Synergistic Antiproliferative Effect of Sinomenine and Carboplatin on Cervical Cancer Hela Cells

目的:研究选择性环氧合酶-2(COX-2)抑制剂青藤碱(sinomenine,SIN)对宫颈癌Hela细胞生长的影响及其与卡铂联合对宫颈癌Hela细胞的协同抑制作用,初步探讨SIN在宫颈癌中的作用机制。方法:MTT法检测SIN及其与卡铂联合对宫颈癌Hela细胞增殖的影响;流式细胞仪检测处理后宫颈癌Hela细胞周期及凋亡的变化。结果:SIN以时间和剂量依赖性特点抑制宫颈癌Hela细胞的增殖,其与卡铂联合对宫颈癌Hela细胞的增殖具有协同抑制作用。流式细胞仪细胞周期分析表明,SIN处理组G1期细胞比例明显增加,S期细胞比例明显减少;卡铂处理组结果相反。细胞凋亡分析表明,SIN处理组细胞凋亡率较对照组升高,呈时间和剂量依赖性特点;两药联合处理组细胞凋亡率较单药处理组升高。结论:SIN以时间和剂量依赖性抑制宫颈癌Hela细胞的增殖,其作用机制与改变细胞周期分布、促进细胞凋亡有关。SIN与卡铂联合对宫颈癌Hela细胞的增殖具有协同抑制作用,其机制可能与共同影响细胞周期分布、促进细胞凋亡有关。

Objecive：To study the effect and mechanism of selective cyciooxygenase-2 （COX-2） inhibitor sinomenine（SIN） on cervical cancer Hela cells, and to explore its synergistic effect with carboplatin on cervical cancer cells. Methods： MTT assay was used to determine the anti-proliferative effect of selective COX-2 inhibitor SIN and its combination with carboplatin on cervical cancer Hela cells. The cell cycle distribution and apoptosis were detected by Flow cytometry. Results： MTT assays showed that SIN inhibited the growth of cervical cancer Hela cells by concentra- tion and time dependence, and synergistic effect appeared when combined with carboplatin. Flow cytometry results demonstrated that the cell cycle was redistributed： the G1-Phase cell fraction was conspicuous increased while the S- Phase cell fraction was significantly decreased after treated with SIN （ P 〈 0.05）. However, the result was opposite after treated with carboplatin. The apoptotic index was increased in SIN group than that in control group, which with time and dose dependence. The apoptotic index was significantly increased after treated with SIN combined with carboplatin.Conclusions：SIN inhibits the growth of cervical cancer cells by concentration and time dependence, the mechanism of which may relate to its cell cycle distribution and apoptosis induction. SIN combined with carboplatin could exert synergistic antiproliferative effect on cervical cancer Hela cells by influencing cell cycle distribution and apoptosis.