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作 者:徐军[1] 孙新[2] 杨晓迪[2] 王媛媛[2] 王芳[1]
机构地区:[1]淮南市第一人民医院检验科,安徽省淮南232007 [2]蚌埠医学院病原生物学教研室,安徽省感染与免疫重点实验室
出 处:《中国基层医药》2009年第11期1946-1948,I0001,共4页Chinese Journal of Primary Medicine and Pharmacy
摘 要:目的观察弓形虫溶解抗原(TLA)对小鼠B16黑色素瘤生长以及肿瘤血管生成的影响。方法20只C57BL/6J小鼠皮下接种B16黑色素瘤细胞,建立荷瘤动物模型,从小鼠荷瘤的第7天开始,每隔2天实验组小鼠经腹腔注射TLA0.1ml,对照组小鼠注射同等剂量0.9%氯化钠注射溶液,荷瘤21d后处死小鼠剥取肿瘤,测量肿瘤体积与重量,计算抑瘤率,免疫组化法检测肿瘤微血管密度(MVD)与血管内皮生长因子(VEGF)表达情况。结果TLA显著抑制了小鼠体内黑色素瘤生长,实验组肿瘤体积与重量明显小于对照组(P〈0.05),抑瘤率为49.6%。实验组与对照组的MVD值分别为(44.4000±4.7888)、(31.9000±2.6012),两组相比较差异有统计学意义(P〈0.05)。实验组肿瘤VEGF表达明显低于对照组(P〈0.05)。结论TLA能够抑制小鼠B16黑色素瘤生长,其抗瘤机制可能与抗血管生成有关。Objective To observe the effects of Toxoplasma lysate antigen(TLA) on growth inhibition and tumor angiogenesis in mice B16 melanoma. Methods Twenty mice bearing B16 melanoma were established by subcutaneous inoculating with B16 cells and were randomly divided into the treatment group and the control group 0. 1 ml TLA was administered once every two days for the treatment group starting on the seventh day after inoculation, and an equivalent volume of sterile saline was administered similarly in the control group. The mice were sacrificed on 21th day after the tumor cells was injected. The anti-tumor effects of TLA were observed by measuring the size and weight of tumor. The microvessel density(MVD) and expression of vascular endotheilial growth factor(VEGF) were observed by immunohistochemieal method. Results TLA can markedly inhibit the B16 melamoa growth in mice. The volume and weight of the tumors in the experimental group were significantly decreased compared with the control group( P 〈 0. 05), and the tumour inhibitory rate was 49.6%. The MVD of experimental group and control was ( 44. 4000 ± 4. 7888) and( 31. 9000 ± 2. 6012) respectively, and with a significant difference between two groups( P 〈 0. 05 ). The VEGF in the treatment group were significantly lower than those in the control group ( P 〈 0.05 ). Conclusion TLA can inhibit the growth of the B16 melanoma in mice, suggesting that the anti-tumor effect induced by TLA via a possible antianigionesis mechanism.
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