摘要
目的探讨单一剂量的美法仑治愈荷瘤野生型C57BL/6小鼠的过程与肿瘤坏死因子α(TNFα)的关系。方法以3种遗传背景相同、肿瘤坏死因子受体1(TNFR1)基因型不同的TNFR1+/+、TNFR1+/-和TNFR1-/-C57BL/6小鼠为实验动物,皮下接种数量相同的小鼠淋巴瘤EL4细胞。接种瘤细胞后12d,给基因型不同的各组荷瘤小鼠腹腔内单次注射7.5mg/kg的美法仑。以荷瘤野生型C57BL/6小鼠(TNFR1+/+)为对照,观察美法仑对荷瘤TNFR1+/-C57BL/6小鼠和荷瘤TNFR1-/-C57BL/6小鼠的治疗效应。结果在美法仑(7.5mg/kg)治疗后的1周内,基因型不同的各组荷瘤小鼠肿瘤消退的速度基本相同。在随后的2月内,荷瘤TNFR1+/+和TNFR1+/-C57BL/6小鼠的肿瘤结节逐渐消退、肿瘤治愈;而多数荷瘤TNFR1-/-C57BL/6小鼠的肿瘤结节缩小后又再次出现并逐渐长大、肿瘤复发。结论TNFα与美法仑治愈肿瘤的过程密切相关,其中美法仑的抗肿瘤作用与荷瘤小鼠TNFR1的表达无关,但在美法仑治疗后,机体预防或避免肿瘤复发方面需要TNFR1在机体细胞的表达,而不是在肿瘤细胞的表达。
AIM： To investigate the relationship between TNFα and tumor rejection induced by a single dose of melphalan in C57BL/6 mice. METHODS： Different gene type mice （TNFR1^＋/＋, TNFR1^＋/- and TNFR1^-/-） with the same genetic background of C57BL/6 were used in this experiment. Murine lymphoma EL4 cells were inoculated subcutaneously into the different gene type mice simultaneously. Twelve days later, 7. 5 mg/kg melphalan was used intraperitoneally to treat the tumor-bearing mice with TNFR1^＋/＋, TNFR1^＋/- and TNFR1^-/-. The tumors in the different gene type mice were observed and recorded every one to three day. RESULTS： After the treatment of 7.5 mg/kg melphalan during the first week, the tumors in the different gene type mice shrank at a similar rate. In the following 2, months, the tumors in the TNFR1^＋/＋ and TNFR1^＋/- C57BL/6 mice gradually shrank and were cured but most tumors in the TNFR1^-/- C57BL/6 mice relapsed after melphalan treatment. CONCLUSION： TNFα plays an important role in melphalan-induced tumor rejection. The anti-tumor effect of melphalan has no relationship with the expression of tumor necrosis factor 1 in tumor-bearing mice. TNFR1 is required to prevent or avoid the relapse of tumors in mice instead of tumor cells.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2007年第4期320-323,共4页
Chinese Journal of Cellular and Molecular Immunology
基金
国家留学基金及辽宁省自然科学基金资助(20062156)
