小鼠机体炎症反应促进纤维肉瘤生长的作用

目的   探讨小鼠机体炎症反应促进纤维肉瘤生长的作用及可能机制。方法   C57BL/6小鼠随机分为正常对照组(PBS组)、脂多糖组(LPS组)、纤维肉瘤组(PC组)、脂多糖+纤维肉瘤组(LC组)、脂多糖+纤维肉瘤+塞来昔布组(Cele组)，PBS组小鼠腹腔注射PBS缓冲液，其余各组小鼠给以脂多糖(LPS)建立炎症模型，实验第5天处死LPS组、PBS组小鼠，其余组小鼠皮下接种纤维肉瘤细胞，同时Cele组小鼠给予塞来昔布，接种肿瘤第21天处死小鼠。比较各组小鼠的一般状况及肿瘤体积，处死小鼠后取肺组织观察外形改变及组织病理学特点，应用CD31染色比较PC组及LC组小鼠肿瘤的血管形态及微血管密度(MVD)。结果   与PBS组相比，LPS组小鼠肺组织血管通透性增高，组织液渗出增多，肺泡腔内可见大量红细胞、炎症细胞；与PC组相比，LC组小鼠肿瘤生长速度快，肿瘤MVD增加，血管紊乱。结论   炎症反应对纤维肉瘤的生长有促进作用，其机制可能与促进肿瘤血管生成有关，抗炎治疗可抑制纤维肉瘤的生长。

Inflammatory response promotes the growth of fibrosarcoma in the mice model

Objective   To study the effects of inflammation on the growth of tumor in fibrosarcoma bearing mice and the possible mechanism. Methods   C57BL/6 mice were randomly divided into 5 groups： the normal control group (PBS group), the lipopolysaccharide group (LPS group), the fibrosarcoma group (PC group), the LPS + fibrosarcoma group (LC group), and the LPS + fibrosarcoma + celecoxib group (Cele group). PBS buffer was intraperitoneally injected to the PBS group mice, and the remaining groups were given lipopolysaccharide (LPS) to establish the inflammation model. The mice of the LPS and PBS groups were killed on the fifth day， and the rest were subcutaneously inoculated with fibrosarcoma cells. Meanwhile the Cele group mice were given celecoxib and the mice were sacrificed 21 days after the inoculation. The general conditions and tumor volumes of the mice were compared. Mice were sacrificed, and the profile changes and the pathological characteristics of the lung tissues were studied. Tumor microvascular density and vessel phenotype of PC group and LC group mice were compared by CD31 staining. Results   Compared with the PBS group, the lung vascular permeability and the tissue fluid exudation increased, and a large number of red blood cells and inflammatory cells were observed in the LPS group. Compared with the PC group， the tumors in the LC group grew faster, the microvascular density increased and the blood vessels were in disorder. Conclusion   The inflammatory response promotes the growth of fibrosarcoma possibly by the promotion of the tumor angiogenesis. Anti inflammatory treatment can inhibit the growth of fibrosarcoma.