中文摘要：

目的：通过在小鼠背侧施加外科切口的方法构建黑色素瘤与急性炎症共存的动物模型，评估急性炎症与肿瘤进程的关系，观察肿瘤不同生长阶段干扰素-γ／转化生长因子-β（IFN-γ/TGF—β）的变化，初步探讨二者相互影响的机制。方法：选用6周龄C57BL雄性小鼠建立黑色素瘤荷瘤动物模型，于左侧鼠蹊部接种B16F10单细胞悬液，分为单纯肿瘤组（对照组）和伤口＋肿瘤组（实验组），待肿瘤生长至0．5cm^3时于实验组小鼠右侧背部构建伤口模型，动态观察肿瘤体积，绘制肿瘤生长曲线，利用ELISA检测血清与肿瘤组织中IFN-γ／TGF—β的表达水平；根据ELISA检测结果，建立注射外源性IFN-γ的动物模型（回收实验），观察TGF—β表达水平的变化。结果：急性炎症对肿瘤的影响呈现为早期抑制阶段与晚期失抑制阶段。在早期抑制阶段，肿瘤生长减缓，IFN-γ高表达，TGF-β低表达；在晚期失抑制阶段，肿瘤生长恢复至正常速度，TGF—β表达升高。外源注射IFN-γ后，肿瘤生长曲线也表现为早期抑制时相和晚期失抑制时相。早期抑制时相中，TGF—β在实验组与对照组表达无显著性差异（P〉0．05）；晚期失抑制时相中，TGF-β在血清及肿瘤中表达明显升高（P〈0．05）。结论：急性炎症初期由于IFN-γ的作用，肿瘤的生长暂时受到抑制，随着时间推移TGF-β表达升高拮抗IFN-γ的抑制作用，使肿瘤获得再生长。

英文摘要：

Objective： To build a mouse tumor model with a manufactured surgical wound representing acute inflammation, and to evaluate the relationship between acute inflammation or wound healing and the process of tumor growth. Then to observe the impact of IFN-γ/TGF-β on tumor growth. Methods： Male C57BL mice of six weeks were used and divided into the experiment group and the control group. The B16F10 melanoma cell suspension was injected into the left groin area of each mouse. A wound measured 1 cm in diameter was built on the opposite side of bodies in the experiment group when tumor volume was about 0.5 cm3. The expression of IFN-γ/TGF-β in blood serum and tumor tissues were examined by ELISA. In order to further confirm the effect of TGF-β on tumor growth, another 16 mice models with melanoma were established and 8 of them received IFN-γ injection （the experiment group）. Results： When acute inflammation had influences on tumor, a two-phase development was presented. In the early phase, the growth of tumor in the mice with wound was slower than that in the control group. In the early phase, the release of IFN-γ was higher and the release of TGF-β was lower in the experiment group. In the later phase, the growth of tumor in the mice with wound was similar to that in the controls and the release of TGF-β was higher. In vivo experiment confirmed the above results. In the early phase, the release of TGF-β was not significantly different between the experiment group and the control group （P〉0.05）. In the later phase, the release of TGF-β in the experiment group was higher than that in the control group （P〈0.05）. Conclusion： In the early phase of acute inflammation, inhibitory effects of IFN-γ on tumor growth were presented. In the later phase, the inhibited tumor was resistant to IFN-γ through the release of TGF-β to balance the effect of inflammatory factors on tumor cells.