小鼠皮下气囊慢性炎症模型的建立

Research of chronic inflammation model of mouse subcutaneous air pouch

目的:探索建立小鼠皮下慢性炎症模型的方法。方法:在小鼠皮下制作气囊,然后向气囊内注入不同致炎物(脂多糖和卡介苗),建立两种慢性炎症模型,观察皮下慢性炎症发生、发展情况及慢性炎症生成率。对照组小鼠气囊内注入生理盐水。结果:实验组小鼠皮下气囊壁慢性炎症生成率均为100%,对照组小鼠气囊壁无慢性炎症反应发生。使用t检验对各组小鼠皮下气囊壁的重量进行统计分析。脂多糖组与对照组相比,在造模后第5、7、12、14和16天时差异有统计学意义(P<0.05);卡介苗组与对照组相比在第5天时差异无统计学意义(P>0.05),在造模后第7、12、14和16天时差异有统计学意义(P<0.05)。脂多糖和卡介苗组的气囊壁均在造模后第7天出现典型的慢性炎症表现。脂多糖和卡介苗组气囊灌洗液的中性粒细胞在造模5 d逐渐为淋巴细胞和单核巨噬细胞取代,对照组灌洗液未检出炎细胞。结论:在小鼠皮下制作气囊,注入脂多糖或卡介苗可以成功地建立小鼠皮下气囊慢性炎症模型。此模型能较好地模拟在单一致炎因子存在情况下引起的慢性炎症状态。

Objective： To investigate the method of establishing subcutaneous chronic inflammation model in mice.Methods： The chronic inflammation was induced by injecting two kinds of proinflammatory substances（Lipopolysaccharide or Bacillus Calmette-Gu） into subcutaneous air pouches of mice.In control mice,saline was injected.The progress of inflammation were recorded.Results： Chronic inflammation was observed in all the mice after treated with proinflammation substances in the subcutaneous air pouch.Significant difference（P0.05） was observed in the subcutaneous air pouch wall weight between the control group and the group of mice treated with lipopolysaccharide in the 5th,7th,12th,14th and 16th day;the subcutaneous air pouch wall weight did not show differences（P0.05） between the control group and the group of mice treated with Bacillus Calmette-Gu in the 5th day,but significant difference（P 0.05） was observed in the 7th,12th,14th and 16th day.Both of the experimental group were observed typical performance of chronic inflammation in the 7th day after the model was made.In the subcutaneous air pouch fluid of experimental group,the neutrophils was insteaded by the mononuclear macrophages and lymphocytes gradually after the model was made 5 days later.Inflammation cells din ’ t be found of in the subcutaneous air pouch fluid of control group.Conclusion： The subcutaneous chronic inflammation model could be established by injecting of lipopolysaccharide or Bacillus Calmette-Gu into the air pouch.The model can simulate the real situation of chronic inflammation induced by single proinflammation substances.