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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。
Objective To investigate the effect and possible mechanism of inflammation in mice on the growth of fibrosarcoma. Methods C57BL / 6 mice were randomly divided into normal control group (PBS group), lipopolysaccharide group (LPS group), fibrosarcoma group (PC group), lipopolysaccharide + fibrosarcoma group (LC group), lipopolysaccharide + fibrosarcoma + Celecoxib group (Cele group). The PBS group mice were intraperitoneally injected with PBS buffer. The remaining mice were given lipopolysaccharide (LPS) to establish the model of inflammation. On the fifth day, mice in LPS group and PBS group were sacrificed. Groups of mice were inoculated subcutaneously with fibrosarcoma cells, while cele group mice were given celecoxib. Mice were sacrificed on day 21 of vaccination. The general condition and tumor volume of mice in each group were compared. After the mice were sacrificed, the lung tissues were taken out to observe the change of appearance and the histopathological features. The tumor morphology and microvessel density (MVD) of mice in PC group and LC group were compared by CD31 staining. Results Compared with PBS group, the mice in LPS group had higher vascular permeability and more exudation of tissue fluid in the lung tissue than those in PBS group. Compared with PC group, mice in LC group had faster tumor growth and tumors MVD increased, vascular disorders. Conclusion Inflammatory reaction may promote the growth of fibrosarcoma. Its mechanism may be related to the promotion of tumor angiogenesis. Anti-inflammatory treatment can inhibit the growth of fibrosarcoma.