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肿瘤坏死因子的抗肿瘤作用及其机理的研究 被引量:2

ANTITUMOR ACTIVITY AND MECHANISM OF ACTION OF TUMOR NECROSIS FACTOR
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摘要 在体内肿瘤坏死因子Tumor Necrosis Factor,TNF)的抗肿瘤效果是剂量依赖的。我们研究发现,移植了S_(180)肉瘤的小鼠从尾静脉输入0.15μg天然的兔TNF即可致使移植瘤明显出血坏死,肿瘤生长抑制,动物存活时间延长,但未见完全治愈。0.3μg兔TNF可使多数动物完全治愈。这种治疗效果与出血坏死程度基本平行。细菌脂多糖(Lipopoly saccharid.LPS)在大于5μg时也能引起肿瘤明显出血坏死,但静脉输入1μgLPS不足以引起肿瘤的出血坏死。这个剂量的LPS与0.15μg TNF合用后协同增强了抗肿瘤作用,部分动物完全治愈。将用LPS和/或TNF完全治愈的小鼠睥细胞(免疫睥细胞)在S_(180)移植同时静脉输入到小鼠体内,结果有6/14的小鼠未长出肿瘤,而输注同样数量正常鼠脾细胞的动物中仅有1/14的小鼠未长出肿瘤,与接种失败率相当。输入免疫脾细胞后,其余长出的肿瘤在前10天生长缓慢,但10天后又恢复到对照水平,这些结果提示TNF的抗肿瘤作用还依赖于内体免疫机能的状态。 Tumor necrosis factor (TNF) possesses dose-dependent antitumor activity in vivo. Our results showed that 0.15 μg of native rabbit TNF can cause obvious he-morrhagical necrosis of 10-day sarcoma 180 (S-180) in mice 24 hr after iv injection, and prolonged survival time of tumor-bearing mice, but none was cured. 75% μ of s-180-bearing mice were cured after administration, of 0.3 μg of TNF. Gure rate was correlated with the degree of tumor hemorrhagical necrosis. Bacterial lipo-poly saccharides (LPS), another agent of tumor hemorrhagical necrosis, had synergistic antitumor effect with TNF. 1 μg of LP-S, which was unable to induce tumor hemorrhage, can enhance antitumor activity of TNF, and a part of tumor-bearing mice received treatment of 0.15 μg of TNF combined with 1 μg of LPS was cured. 6/14 of mice did not suffer from tumor in mice which were treated with transfer immunity of spleen cells from TNF-cured mice shortly after tran splantation of s-180. Growth rate of the tumors in the remained 8/14 mice was recovered to control level from 5-10 days suppression after adoptive immunity treatment It is suggested that TNF can provoked antitumor immunity of host and antitumor effect of TNF was eventually dependent on the state of host immune function.
出处 《癌症》 SCIE CAS CSCD 北大核心 1991年第1期12-15,共4页 Chinese Journal of Cancer
关键词 肿瘤坏死因子 抗肿瘤作用 Tumor Necrosis Factor Lipopoly sacch arid
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