摘要
目的探讨表没食子儿茶素没食子酸酯(EGCG)联合紫杉醇对肝癌Hep G2细胞增殖及荷瘤裸鼠肿瘤生长的抑制作用。方法将Hep G2细胞分为对照组、EGCG组、紫杉醇组、EGCG联合紫杉醇组。噻唑蓝法观察不同药物干预对Hep G2细胞增殖的抑制作用,流式细胞术检测Hep G2细胞凋亡。构建肝癌细胞体外肿瘤球,比较各组药物对肿瘤球生长的抑制作用。构建裸鼠肝癌异位肿瘤模型,比较各组裸鼠肿瘤生长抑制率。结果给药24、48 h后,EGCG组、紫杉醇组、EGCG联合紫杉醇组Hep G2细胞增殖抑制率显著高于对照组(P<0.01),EGCG联合紫杉醇组Hep G2细胞增殖抑制率显著高于EGCG组和紫杉醇组(P<0.01)。EGCG组、紫杉醇组、EGCG联合紫杉醇组Hep G2细胞凋亡率显著高于对照组(P<0.01),EGCG联合紫杉醇组Hep G2细胞凋亡率显著高于EGCG组和紫杉醇组(P<0.01)。EGCG组、紫杉醇组、EGCG联合紫杉醇组Hep G2细胞肿瘤球生长抑制显著高于对照组(P<0.01),EGCG联合紫杉醇组Hep G2细胞肿瘤球生长抑制显著高于EGCG组和紫杉醇组(P<0.01)。EGCG组、紫杉醇组、EGCG联合紫杉醇组荷瘤裸鼠肿瘤质量显著低于对照组(P<0.01),EGCG联合紫杉醇组荷瘤裸鼠肿瘤质量显著低于EGCG组和紫杉醇组(P<0.01)。EGCG组、紫杉醇组、EGCG联合紫杉醇组荷瘤裸鼠肿瘤生长抑制率显著高于对照组(P<0.01),EGCG联合紫杉醇组荷瘤裸鼠肿瘤生长抑制率显著高于EGCG组和紫杉醇组(P<0.01)。结论 EGCG联合紫杉醇能够有效抑制肝癌细胞的增殖和肿瘤的生长。
Objective To explore the inhibition of epigallo catechin gallate( EGCG) combined with paclitaxel on Hep G2 cell multiplication and tumor growth in bearing cancer nude mice. Methods The Hep G2 cells were divided into control group,EGCG group,paclitaxel group,EGCG combined with paclitaxel group. The depressant effect of different drugs on Hep G2 cell multiplication was detected by methylthiazolyldiphenyl-tetrazolium bromide assay. The apoptosis of Hep G2 cell was detected by flow cytometry. The tumor spheres were constructed with Hep G2 cell in vitro,then the inhibition of drug on tumor sphere growth was compared in the groups. Hep G2 cells were xenografted in mice to establish the animal models,then the inhibition rate of tumor growth in nude mice was compared in the groups. Results Twenty-four and forty-eight hours after drug intervention,the inhibition rate of Hep G2 cells multiplication in EGCG group,paclitaxel group and EGCG combined with paclitaxel group was significantly higher than that in control group( P〈0. 01); the inhibition rate of Hep G2 cells multiplication in EGCG combined with paclitaxel group was significantly higher than that in EGCG group and paclitaxel group( P〈0. 01). The apoptosis rate of Hep G2 cells in EGCG group,paclitaxel group and EGCG combined with paclitaxel group was significantly higher than that in control group( P〈0. 01); the apoptosis rate of Hep G2 cells in EGCG combined with paclitaxel group was significantly higher than that in EGCG group and paclitaxel group( P〈0. 01). The depressant effect of Hep G2 tumor sphere growth in EGCG group,paclitaxel group and EGCG combined with paclitaxel group was significantly higher than that in control group( P〈0. 01); the depressant effect of Hep G2 tumor sphere growth in EGCG combined with paclitaxel group was significantly higher than that in EGCG group and paclitaxel group( P〈0. 01). The tumorous weight of bearing cancer nude mice in EGCG group,paclitaxel group and EGCG combined with paclitaxel group was significantly lower than that in control group( P〈0. 01); the tumorous weight of bearing cancer nude mice in EGCG combined with paclitaxel group was significantly lower than that in EGCG group and paclitaxel group( P〈0. 01). The inhibition rate of tumor growth of bearing cancer nude mice in EGCG group,paclitaxel group and EGCG combined with paclitaxel group was significantly higher than that in control group( P〈0. 01); the inhibition rate of tumor growth of bearing cancer nude mice in EGCG combined with paclitaxel group was significantly higher than that in EGCG group and paclitaxel group( P〈0. 01). Conclusion EGCG combined with paclitaxel can effectively inhibit the proliferation of Hep G2 cells and the tumor growth.
出处
《新乡医学院学报》
CAS
2015年第3期216-219,共4页
Journal of Xinxiang Medical University