Caveolin-1/MCP-1/IL-12在LPS诱导的急性肺损伤模型中的作用

Roles of Caveolin-1,MCP-1 and IL-12 in a Mouse Model of Acute Lung Injury Induced by Lipopolysaccharide

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0.9%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m RNA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m RNA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-1 in 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.