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目的 了解血管内皮细胞生长因子 (vascularendothelialgrowthfactor,VEGF)可溶性受体sFlt 1联合内皮抑素 (Endostatin ,ES)基因治疗对甲状腺滤泡状癌细胞生长的影响 ,并探讨其作用机理。方法 2 0 0 1年 6月至 2 0 0 3年 12月 ,采用表达ES的肿瘤细胞系FTC133 rvEndo和表达sFlt 1的 2 93 Flt1 3d细胞行动物实验 ,观察肿瘤在裸鼠模型中的生长状况。用抗CD31抗体对肿瘤切片进行免疫组织化学染色检测微血管 ,计算微血管密度 (microvesseldensity ,MVD)。检测血清中ES和VEGF浓度。结果 在裸鼠模型中 ,种植 2 8d后 ,抑瘤率sFlt1组为 70 37% ,sFlt1+ES组为 93 4 9%。免疫组化染色表明对照组MVD为 (10 2 71± 13 14 ) ;而sFlt1组为(40 76± 12 6 5 ) ,sFlt1+ES组为 (13 71± 6 2 7) ,各组间差异有显著性 (P <0 0 5 )。对照组带瘤鼠血清中人VEGF浓度为 (31 2 5± 6 2 1) pg ,而sFlt1组为每毫升 (10 5 9± 0 72 ) pg ,sFlt1+ES组为每毫升 (7 4 5± 0 81) pg ,后两者与对照组间差异有显著性 (P <0 0 5 )。结论 sFlt1和ES的联合应用可增强其抗肿瘤血管生成和抗甲状腺滤泡状癌肿瘤生长的作用。其机理可能与VEGF的受抑制有关。
Objective To investigate the effects of soluble vascular endothelial growth factor (VEGF) sFlt 1 and endostatin (ES) gene therapy on the growth of thyroid follicular carcinoma cells and to explore its mechanism. METHODS: From June 2001 to December 2003, the tumor-bearing mice were treated with FTC133 rvEndo expressing ES and 2 93 Flt1 3d cells expressing sFlt 1 . Tumor sections were examined by immunohistochemistry with anti-CD31 antibody for the detection of microvessels, and the microvessel density (MVD) was calculated. Serum ES and VEGF concentrations were measured. Results In the nude mouse model, the growth inhibition rate was 70 37% in the sFlt1 group and 93 49% in the sFlt1 + ES group after 28 days of planting. Immunohistochemical staining showed that the MVD was (10 2 71 ± 13 14) in the control group, (40 76 ± 12 6 5) in the sFlt1 group, and (13 71 ± 6 27) in the sFlt1 + ES group Significance (P <0 05). In the control group, the concentration of human VEGF in the tumor-bearing mice was (31 2 5 ± 6 2 1) pg, while in the sFlt1 group was 1059 ± 0 72 pg ml sFlt1 + ES group was 74 500 0 81) pg, the difference between the latter two groups and the control group was significant (P <0 05). Conclusion The combination of sFlt1 and ES can enhance its anti-tumor angiogenesis and anti-thyroid follicular carcinoma growth. The mechanism may be related to the inhibition of VEGF.