摘 要: 通过实时荧光定量PCR (real-time PCR)等方法, 研究了脂多糖(lipopolysaccharide, LPS)诱导的急性肺损伤(acute lung injury, ALI)小鼠模型肺组织中小窝蛋白-1 (caveolin-1)、血管细胞粘附分子-1 (vascular cell adhesion molecule-1, VCAM-1)和E-选择素(E-selectin)的mRNA表达变化情况, 以初步探索caveolin-1在ALI发病机制中的作用。实验结果表明, 与对照组相比较, 经腹腔注射LPS (20 mg/kg)的实验组中肺系数、髓过氧化物酶(myeloperoxidase, MPO) mRNA水平明显升高(P<0.05), 同时VCAM-1和E-selectin的mRNA表达水平增加(P<0.05), 而caveolin-1的mRNA表达减少(P<0.05)。上述研究提示, LPS可能通过抑制caveolin-1的表达, 使黏附分子VCAM-1、E-selectin的表达上调, 从而使肺组织中性粒细胞大量浸润, MPO增多, 加重肺损伤。

Abstract: The real-time fluorescence quantitative PCR (real-time PCR) was used to study the expression of caveolin-1, vascular cell adhesion molecule-1 (VCAM-1) and E-selectin in the mouse model of lipopolysaccharide (LPS)-induced acute lung injury (ALI), so as to explore the possible role of caveolin-1 in the pathogenesis of ALI. The results demonstrated that compared with the control group, the lung index and myeloperoxidase (MPO) mRNA in the LPS group were significantly higher than those in the control group (P<0.05). The VCAM-1 and E-selectin mRNAs were increased in the lungs of the LPS group (P<0.05), while the caveolin-1 mRNA was decreased. These data suggested that LPS possibly induced the neutrophil infiltration and damage to lung tissue by decreasing caveolin-1 and by increasing the expression of adhesion molecules VCAM-1 and E-selectin.