中文摘要：

目的：探讨黄岑苷对宫颈癌细胞株He La的放射增敏作用及机制。方法：MTT法检测不同浓度黄岑苷对He La细胞的活力抑制能力,并计算IC50筛选实验药物浓度;克隆形成实验检测放射组与联合组在不同照射剂量下细胞的放射增敏作用;流式细胞术检测单药组、放射组与联合组的细胞周期变化;Western blot检测不同组细胞中Akt、p-Akt、Bad和p-Bad的蛋白水平。结果：黄岑苷呈浓度依赖性抑制He La细胞的活力,IC50为43.65 mg/L,采用20%IC50浓度8 mg/L进行放射增敏实验。克隆形成实验结果显示8 mg/L黄岑苷联合放射治疗可使生存曲线左移,D0、Dq值显著小于放射组（P〈0.05）。流式细胞仪检测结果显示黄岑苷阻滞He La细胞于G2/M期。联合组细胞中p-Akt和p-Bad的蛋白水平均显著高于其它各组（P〈0.05）。结论：黄岑苷对He La细胞具有放射增敏作用,其机制可能与其阻滞细胞于G2/M期和活化PI3K/Akt信号通路有关。

英文摘要：

AIM： To investigate the effect of baicalin on the radiosensitization of He La cells. METHODS：The cell activity was determined by MTT assay. The radiosensitivity of He La cells was detected by colony formation assay.The cell cycle was analyzed by flow cytometry. The protein levels of Akt,p-Akt,Bad and p-Bad were examined by Western blot. RESULTS： The cell growth of the He La cells was inhibited by baicalin dose-dependently and IC50 was 43. 65 mg / L.The results of colony formation assay showed that combination of 8 mg / L baicalin and radiotherapy further improved survival curve and decreased the value of D0 and Dq,as compared with radiotherapy alone（ P〈0. 05）. Furthermore,baicalin enhanced the effect of radiotherapy on cell cycle,as evidenced by the increase in cell percentage in G2/ M phase（ P〈0. 05）.Additionally,after incubation with baicalin,radiotherapy-induced phosphorylation of Akt and Bad were further augmented（ P〈0. 05）. CONCLUSION： Baicalin augments radiosensitivity of He La cells through the inhibition of cell cycle transition and activation of PI3 K / Akt signaling pathway.