论文部分内容阅读
目的:探讨巨噬细胞炎症蛋白2(MIP2)在内毒素性急性肺损伤(ALI)中的可能作用。方法:采用斑点杂交及原位杂交技术对ALI大鼠肺组织中MIP2mRNA的表达进行定量和定位研究。结果:内毒素性ALI时大鼠各时点肺组织MIP2mRNA表达量显著高于对照组,且与血浆及肺组织匀浆髓过氧化酶(MPO)活性呈正相关(r=0.729,0.885,P均<0.05)。原位杂交发现,在ALI早期,肺内巨噬细胞是MIP2的主要分泌细胞。结论:在ALI早期,巨噬细胞释放的MIP2可能是ALI时多形核白细胞(PMN)在肺内大量浸润并激活的原因之一。
Objective: To investigate the possible role of macrophage inflammatory protein 2 (MIP2) in endotoxin-induced acute lung injury (ALI). Methods: The expression of MIP2 mRNA in lung tissue of ALI rats was quantitatively determined by dot blot hybridization and in situ hybridization. Results: The expression of MIP2 mRNA in lung tissue of endotoxin-exposed ALI rats at each time point was significantly higher than that of the control group, and positively correlated with the activity of myeloperoxidase (MPO) in plasma and lung homogenate (r = 0.729,0. 885, P <0.05). In situ hybridization found that in the early stage of ALI, intrapulmonary macrophages were the major secretory cells of MIP2. CONCLUSIONS: MIP2 released by macrophages may be one of the reasons for the massive infiltration and activation of polymorphonuclear leukocytes (PMNs) in the lungs during ALI.