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目的:通过对肺癌小鼠腹腔巨噬细胞的活性和5种细胞因子表达量研究,探讨细颗粒物(Particulate Matter 2.5,PM2.5)的作用机制。方法:尾静脉注射法建立肺癌荷瘤小鼠模型,30只随机分为3组:荷瘤对照组、PM2.5暴露组(气管滴注法暴露PM2.5)、NS暴露组(滴注等量生理盐水)。中性红比色法检测PM2.5对肺癌小鼠腹腔巨噬细胞活性的影响;ELISA法检测血清和腹腔巨噬细胞培养液上清中IL-2、IL-10、TNF-α、IFN-γ和MIF 5种细胞因子的表达情况。结果:腹腔巨噬细胞吞噬能力实验结果显示,PM2.5暴露组和NS暴露组分别与荷瘤对照组比较,吞噬活性显著提高(P<0.05),PM2.5暴露组明显高于NS暴露组(P<0.05)。以上3组吞噬率间两两比较均具有统计学差异(P<0.05)。ELISA结果显示,血清和巨噬细胞细胞培养液上清中IL-2和MIF的表达量显著降低,IL-10表达量显著升高(P<0.05)。而TNF-α在血清中的表达量显著降低,但在细胞培养液上清中的表达量显著增高(P<0.05)。结论:空气细颗粒物暴露对荷瘤肺癌小鼠腹腔巨噬细胞的活性虽然具有上调作用,但同时损伤了巨噬细胞和机体的非特异性免疫和特异性免疫功能。
Objective: To investigate the mechanism of action of Particulate Matter 2.5 (PM2.5) on the activity of peritoneal macrophages and expression of five cytokines in lung cancer mice. Methods: Tumor-bearing mice model of lung cancer was established by tail vein injection. Thirty mice were randomly divided into 3 groups: tumor-bearing control group, PM2.5 exposure group (tracheal instillation PM2.5 exposure), NS exposure group Normal saline). The effect of PM2.5 on the activity of peritoneal macrophages in lung cancer mice was detected by neutral red colorimetric method. The levels of IL-2, IL-10, TNF-α and IFN- γ and MIF 5 kinds of cytokines expression. Results: The phagocytosis of peritoneal macrophages showed that the phagocytic activity of PM2.5-exposed group and NS-exposed group was significantly higher than that of tumor-bearing control group (P <0.05), and the PM2.5-exposed group was significantly higher than that of NS-exposed group (P <0.05). The above three groups of phagocytosis rates were statistically significant (P <0.05). ELISA results showed that the expression of IL-2 and MIF in serum and macrophage cell culture supernatant decreased significantly, and the expression of IL-10 increased significantly (P <0.05). However, the expression of TNF-α in serum was significantly decreased, but the expression of TNF-α was significantly increased in the supernatant (P <0.05). CONCLUSION: Although the airborne particulate exposure has an upregulation effect on peritoneal macrophages in mice with tumor-bearing lung cancer, it also damages the nonspecific and specific immune functions of macrophages and the body.