目的：本研究在脂多糖（LPS）诱导的急性肺损伤（ALI）小鼠模型上，观察了肺组织中单核细胞趋化蛋 白-1（MCP-1）、炎症介质白介素-12（IL-12）以及小窝蛋白-1（caveolin-1）的表达变化，以初步探索MCP-1 等因子在 ALI 发病机制中的作用。方法：小鼠建模：将小鼠随机分为两组，给予LPS（20mg/kg，i.p）或等体积0. % Nacl 溶液（i.p）处理8 小时；通过观察肺组织外观、病理切片HE 染色、计算肺系数及肺湿重干重比检验模型是否建立成功；通过实时荧光定量 PCR（real-time PCR）以及Western 印迹分析检测MCP-1、IL-12、caveolin-1 的mRNA 和蛋白水平变化。结果：LPS 组的肺湿重干重比、肺系数明显升高，MCP-1、IL-12 的蛋白及mRNA 水平增加，caveolin-1 蛋白水平增高。结论：LPS 可能通过增加肺组织中MCP-1 的表达从而促进肺内巨噬细胞的激活及浸润，增加IL-12的产生，推动ALI 的发生发展，caveolin-1 可能参与了此调节过程。

Objective To explore the possible roles of monocyte chemotactic protein 1(MCP-1), Interleukin 12(IL-12) and caveolin-1in the mouse model of lipopolysaccharide (LPS) -induced acute lung injury (ALI). Methods Mice were randomly divided into two groups, each group mice were treated intraperitoneally (i. p. ) with LPS (20 mg/kg) or sterile 0.9% Nacl solution for 8 h. The immunohistology analysis was used to observe the pathological changes in the lung tissue. The ratio of the W/D weight and the lung coefficient was calculated to assess the tissue edema. The real-time fluorescence quantitative PCR (realtime PCR) and Western Blotting were used to detect the expression of MCP-1, IL-12 and caveolin-1. Results The lung coefficient and lung wet/dry weight ratio of the LPS group were significantly higher than those in the control group. The expression of MCP-1, IL-12 and caveolin-1 were increased in the lungs of the LPS group. Conclusion LPS induced MCP-1 expression, which activated and recruited more inflammatory monocytes to the lungs, increased the expression of IL-12 to promote the development of ALI, and caveolin-1 may be involved in the regulationprocess.