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