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目的 研究血管内皮抑素转基因双歧杆菌口服冻干粉剂 (endostatintransfectedbifido bacteriumoralpowderpreparation ,ETB 2 )对小鼠HAC肝癌细胞皮下移植模型的抑瘤作用 ,探讨其抑瘤机制。方法 小鼠HAC肝癌细胞株皮下接种模型 ,实验组分接种细胞后 2 4h(ETB 2A)和 1周 (ETB 2B)两个时段给药。动物处死后剥离肿瘤 ,称重并计算抑瘤率。苏木精 伊红和EnvisionSystem免疫组化方法 ,分别计数微血管密度 (MVD)、增殖细胞核抗原 (PCNA)指数和血管内皮生长因子 (VEGF)阳性率 ,分析它们同ETB 2抑瘤效应之间的关系。结果 实验组抑瘤率ETB 2A为 5 1.0 6 % ,ETB 2B为39 .10 %。实验组MVD ,ETB 2A为 8.10± 2 .0 3 ,ETB 2B为 12 .0 2± 1.5 4,显著低于对照组 (P <0 .0 5 )。VEGF阳性率ETB 2A为 4.2 0± 1.5 1,ETB 2B为 4.5 0± 2 .82 ,同对照组相比差异有显著性 (P <0 .0 5 )。PCNA指数实验组有降低趋势 ,但差异无显著性。结论 ETB 2可显著抑制小鼠肝癌的生长和发展 ,并有一定的时效关系 ,其可能的抑瘤机制为抑制肿瘤血管增殖 ,使肿瘤坏死增加 ,肿瘤体积减小
Objective To study the anti-tumor effect of endostatin transfected bifidobacterium oral powder preparation (ETB 2 ) on the subcutaneous transplantation model of mouse HAC hepatoma cells, and to explore its anti-tumor mechanism. Methods A subcutaneous model of mouse HAC hepatoma cell line was inoculated. The experimental components were administered at 24 h after inoculation with cells (ETB 2A) and 1 week (ETB 2B). After the animals were sacrificed, the tumors were detached, weighed and the tumor inhibition rate was calculated. Using hematoxylin eosin and Envision System immunohistochemistry methods, the microvessel density (MVD), proliferating cell nuclear antigen (PCNA) index, and vascular endothelial growth factor (VEGF) positive rate were counted, respectively, and the relationship between them and the antitumor effect of ETB 2 was analyzed. . Results The inhibitory rate of ETB 2A in the experimental group was 5 1.06%, and that of ETB 2B was 39.10 %. The MVD, ETB 2A in the experimental group was 8.10±2.03, and ETB 2B was 12.02±1.54, which was significantly lower than that of the control group (P < 0.05). The positive rate of VEGF in ETB 2A was 4.2 0±1.5 1, and ETB 2B was 4.5 0± 2.82. There was a significant difference compared with the control group (P < 0.05). The experimental group of PCNA index had a decreasing trend, but the difference was not significant. Conclusion ETB 2 can significantly inhibit the growth and development of liver cancer in mice and has a certain time-effect relationship. Its possible mechanism of tumor inhibition is inhibition of tumor vascular proliferation, increase of tumor necrosis, and decrease of tumor volume.