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IL-18对Lewis肺癌小鼠Th1/Th2细胞平衡的调节及其抗肿瘤作用的研究

Effect of IL-18 on the Th1/Th2 balance and its antitumor mechanism in C57BL/6 mice Lewis lung cancer

摘要目的 探讨IL-18对Lewis肺癌小鼠Th1/Th2细胞平衡的调节及其抗肿瘤作用的可能机制.方法 C57BL/6小鼠24只,按随机数字法分为IL-18治疗组(A组)、荷瘤模型组(B组)、正常对照组(C组),每组8只,A组、B组复制Lewis肺癌模型,并分别给予IL-18、生理盐水于接种第7日起腹腔注射,C组则正常饲养未予处理.应用酶联免疫吸附法(ELISA)检测各组小鼠血清Th1细胞因子IFN-γ、Th2细胞因子IL-4浓度;观察IL-18对小鼠健康状况、移植瘤体积变化及瘤重的影响.结果 Th1细胞因子IFN-γ浓度A组、C组明显高于B组,差异有统计学意义(P<0.05),Th2细胞因子IL-4浓度A组、C组明显低于B组,差异有统计学意义(P<0.05),而A组与C组两项指标比较差异均无统计学意义(P>0.05).IL-18对小鼠健康状况无明显影响,但对小鼠移植瘤生长有明显抑制作用,肿瘤抑制率为75%.结论 IL-18可诱导IFN-γ而抑制IL-4产生,调节Th1/Th2细胞平衡,从而增强机体免疫应答,有效地控制肿瘤增殖生长.

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abstractsObjective To investigate the effect of Intedeukin-18 (IL-18) on Th1/Th2 balance and its antitumor mechanism in C57BL/6 mice Lewis lung cancer model. Methods 24 C57BL/6 mice were randomly divided into three equal groups: group A(IL-18 injec-tion group, n = 8), group B (Lewis lung cancer model, n = 8) and group C (normal control group, n = 8). The Lewis lung cancer cells were cultured and implanted subcutaneously into the group A and group B. IL-18 and NS were given to group A and B respectively by intrap-eritoneal injection on the 7th day (once every day, 7 times altogether), but group C was not given any treatment. Enzyme-linked immunosor-bent assay (ELISA) was used to detect the Th1/Th2 cytokines. Health status in all the animals was evaluated; the volume and weight ofsubcutaneous tumors were measured. Results The concentration of IFN-γ in group A and C were significantly higher than those in group B (P <0.05), and the concentration of IL-4 in group A and C were significantly lower than those in group B (P<0.05), but there was no significant difference between group A and C (P>0.05). The tumor growth inhibitory rate was 75%. Conclusion IL-18 can effectively induced IFN-γ and inhibit IL-4 production, regulate Th1/Th2 balance in the C57BL/6 mice Lewis lung cancer model, and elicit the antitu-mor immunity of the host, which could obviously inhibit the growth of tumor cells and decelerate the proliferation of tumor cells.

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