染料木黄酮对喉癌Hep_2细胞系增殖和凋亡的影响.pdfVIP

624 中国耳鼻咽喉头颈外科 / 2014年12月，第21卷，第12期 - 染料木黄酮对喉癌Hep 2细胞系增殖和凋亡的影响 1 1 2 2 2 2 周渝 ，王惠民，渠晓丽，原红艳，刘平，张淑香 1 河北医科大学研究生学院，河北　石家庄　050017；2 武警后勤学院附属医院耳鼻咽喉头颈外科，天津　300162 [摘　要］　目的　探讨染料木黄酮（genistein ，Gen ）对人 Tianjin, 300162, China 鳞状细胞喉癌Hep-2细胞系增殖和凋亡的影响。 　用 Cor respondi ng author: ZH A NG Shu xiang(Email: 方法 CCK-8法检测不同浓度Gen对Hep-2细胞系增殖的影响；用 zhang78754@163.com) 实时荧光定量聚合酶链反应（Real-Time PCR ）检测Gen对 [ABSTR ACT]　OBJECTIVE　To investigate the Hep-2细胞系血管内皮生长因子受体-3 （vascular endothelial influence of Genistein (Gen) on proliferation and apoptosis growth factor receptor-3，VEGFR-3 ）mRNA表达的影响； of Hep-2 cell. METHODS　The proliferation of Hep-2 cell 用流式细胞术检测Gen单独及联合VEGFR-3特异性阻滞剂 after treated with various concentrations Gen was detected. MAZ51对Hep-2细胞系凋亡的影响；Western blot检测各组 The changes of VEGFR-3 mRNA were detected by real-time AKT蛋白表达及其磷酸化水平。 　Gen可抑制Hep-2细 polymerase chain reaction (Real-Time PCR) in Hep-2 cells 结果 胞系增殖，且抑制作用呈剂量依赖性；Gen能抑制Hep-2细 treated by Gen. Using flow cytometry (FCM), the variation 胞系的VEGFR-3 mRNA表达，抑制率为32% ；单用Gen和 of cell apoptosis rate after treating Gen alone or Gen MAZ51均能诱导Hep-2细胞系凋亡，二者联合应用对Hep-2 combined with MAZ51(a VEGFR-3-specific blocker) were 细胞系的凋亡诱导作用明显增强；Gen与MAZ51均能抑制 measured. AKT proteins expression and phosphorylation AKT第308位苏氨酸（Thr308）及第473位丝氨酸（Ser473） were determined by Western blot. RESULTS　CCK-8 磷酸化激活，使p-AKT-Thr308和p-AKT-Ser473减少，两种 assay showed the proliferation inhibition on Hep-2 cells had 药物合用抑制率更高。 　Gen可通过抑制VEGFR-3表 a dose-dependent effect treated by Gen. Gen could inhibit 结论 达阻止AKT磷酸化激活，并发挥抑制喉癌细胞增殖和诱导 the expression of VEGFR-3 mRNA, and the inhibition rate 其凋亡的抗癌作用。