红花多糖对人宫颈癌Hela细胞增殖和VEGF表达的影响

目的:通过研究红花多糖对人宫颈癌Hela细胞增殖和血管内皮生长因子(VEGF)表达情况的影响,探讨红花多糖抗宫颈癌作用的分子机制。方法:体外培养人宫颈癌Hela细胞,加入含不同质量浓度(0.02,0.04,0.08,0.16,0.32,0.64和1.28 g·L-1)红花多糖的培养液,培养48 h,用四甲基偶氮唑蓝(MTT)法检测红花多糖对Hela细胞增殖的影响;以不同质量浓度(0.16,0.32,0.64 g·L-1)的红花多糖处理Hela细胞48 h,酶联免疫吸附试验(ELISA)检测细胞上清液中VEGF的表达,实时定量荧光聚合酶链式反应(Real-time PCR)检测VEGF mRNA的表达,免疫印迹法(Western blot)检测VEGF蛋白表达的变化。结果:与空白组比较,(0.16,0.32,0.64 g·L-1)的红花多糖作用于宫颈癌Hela细胞48 h后能显著抑制细胞的体外增殖,呈现剂量依赖性(P0.05)。红花多糖能明显下调Hela细胞VEGF mRNA和蛋白的表达(P0.05)。结论:红花多糖可通过抑制VEGF的表达抑制宫颈癌Hela细胞的增殖,发挥抗肿瘤作用。

Effect of Safflower Polysaccharide on Proliferation and VEGF Expression of Human Cervical Cancer Hela Cells

Objective: To investigate the effect of safflower polysaccharide on proliferation and vascular endothelial growth factor (VEGF) expressions of human cervical cancer Hela cells, and discuss its molecular mechanism against cervical cancer. Method: Human cervical cancer Hela cells were cultured in vitro with different concentrations of safflower polysaccharide (0.02, 0.04, 0.08, 0.16, 0.32, 0.64, 1.28 g·L^-1) for 48 hours. Their effect on Hela cells proliferation was assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Hela cells were treated with different concentrations of safflower polysaccharide (0.16, 0.32, 0.64 g·L^-1) for 48 hours, and then enzyme linked immunosorbent assay (ELISA) was used to detect the VEGF expression in cells supernatant;reverse Real-time PCR was used to detect VEGF mRNA expressions and Western blot method was used to detect VEGF protein expressions. Result: Compared with the blank group, safflower polysaccharide (0.16, 0.32, 0.64 g·L^-1) could significantly inhibit the proliferation of Hela cells after 48 h treatment in a dose-dependent manner (P<0.05). Safflower polysaccharide could significant down-regulate mRNA expressions and protein expressions of VEGF of Hela cells, with significantly statistical differences (P<0.05). Conclusion: Safflower polysaccharide can inhibit proliferation of cervical cancer Hela cells and have its antitumor effect by inhibiting the expressions of VEGF.