中文摘要：

目的观察抗血管生成药物恩度联合放疗对乏氧诱导因子-1α（HIF-1α）和葡萄糖转运蛋白-1（GLUT-1）的影响，并对其联合作用机制进行探讨。方法建立Lewis肺癌移植瘤模型，将32只成瘤小鼠随机分为4组，分别为空白对照组，Endostar组（ES组），放射治疗组（RT组）及Endostar＋放射治疗组（ES＋RT组）。从治疗当天开始，测量肿瘤最长直径（a）及最短直径（b），绘制肿瘤生长曲线，用Western-blot方法对各处理组肿瘤组织中HIF-1α及GLUT-1的表达情况进行检测。结果（1）在对小鼠的肿瘤生长抑制情况方面， ES＋RT组与空白对照组相比，差异具有统计学意义（P〈0.05）， ES＋RT组和ES组之间差异有统计学意义（P〈0.05）。（2）以空白对照组为参照，ES组、RT组、ES＋RT组GLTU-1蛋白的表达呈下降趋势，差异均具有统计学意义（P〈0.05）；ES＋RT组下降最明显，分别与ES组、RT组比较差异均具有统计学意义（P〈0.05）；（3）以空白对照组为参照，ES组、RT组、ES＋RT组的HIF-1α蛋白表达量均下降明显，与空白对照组比较，RT组、ES＋RT组具差异具有统计学意义（P〈0.05），RT组与ES＋RT组之间的差异具有统计学意义（P〈0.05）。（4）HIF-1α与GLTU-1表达呈正相关（P〈0.01）。结论恩度联合放疗能够抑制Lewis 肺癌荷瘤小鼠肿瘤的生长，通过抑制HIF-1α和GLTU-1蛋白的表达，改善肿瘤组织内乏氧状况和酸性微环境，可能是放疗增敏作用的机制之一。

英文摘要：

Objective To observe the effect of anti - angiogenesis drug Endostar on the expressions of hypoxia inducible factor- 1α（ HIF-1α）and glucose transporter- 1 （GLUT- 1 ）, Methods The transplantation tumor models of Lewis lung carcinoma were randomly divided into 4 groups, namely control group, ES group, RT group and ES ＋ RT group. We measured the longest diameter of the tumor （a） and shortest diameter （b）. The tumor volume was calculated by V = ab2/2. The tumor body was for detection. Detection was performed by western blot method. Results （ I ） There was significant difference between ES ＋ RT group and ES group （P 〈 0.05 ）. The combined group inhibited the best. （2）ES ＋ RT group decreased obviously compared with ES group and RT group. The difference was statistically significant （ P 〈 0.05 ）. RT group, compared with ES group, is lower with statistics differences （ P 〈 0.05 ）. （3） ES ＋ RT group has statistical significance （ P 〈 0.05 ）. ES group, the difference was not significant（P 〉0.05 ）. There was significant difference between group RT and group ES ＋ RT（ P 〈 0.05 ）. （4） HIF -1α was positively correlated with GLTU - 1 expression （ P 〈 0.01 ）. Conclusion Endostar combined with radiotherapy can inhibit Lewis mice tumor growth. Endostar can improve the hypoxic tumor which inhibiting the expression of HIF - 1α and GLTU - 1. It may be one of the mechanism for increasing radiosensitization.