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目的和方法：采用斑点及原位杂交方法，检测内毒素性急性肺损伤（ ＡＬＩ） 大鼠肺组织巨噬细胞炎症蛋白－ ２（ ＭＩＰ－ ２） ，单核细胞趋化蛋白－ １（ ＭＣＰ－ １） ｍ ＲＮＡ 表达，观察脂多糖（ＬＰＳ） 刺激猪肺血管内巨噬细胞（ＰＩＭ） ＭＩＰ－ ２ｍＲＮＡ 表达，及其培养上清肿瘤坏死因子α（ＴＮＦα） 、白介素－ ８（ＩＬ－ ８） 含量变化，探讨肺损伤的机制。结果：ＡＬＩ 鼠肺组织ＭＩＰ－ ２ 、ＭＣＰ－ １ ｍ ＲＮＡ 表达显著增加，分别于致伤后３ ｈ 和６ ｈ 达峰值（ Ｐ＜ ０－０１） ；血浆及肺组织匀浆髓过氧化物酶（ ＭＰＯ） 活性亦显著增加，但峰值靠后；肺组织ＭＩＰ－ ２ ｍ ＲＮＡ 表达与血浆及肺匀浆ＭＰＯ 活性呈显著正相关（ Ｐ＜ ０－０５） 。原位杂交显示肺巨噬细胞（ Ｍ） 是ＭＩＰ－ ２ 的主要分泌细胞。ＬＰＳ 刺激的ＰＩＭ 分泌ＴＮＦα早，ＩＬ－ ８ 则晚而长。结论：肺Ｍ通过分泌ＭＩＰ－ ２ 、ＴＮＦα、ＩＬ－ ８ 等在ＡＬＩ 发生、发展中可能起重要作用
PURPOSE AND METHODS: The expression of MIP-2, MCP-1 in lung tissue of endotoxin-induced acute lung injury (ALI) rats was detected by dot blot and in situ hybridization 1) m RNA expression was observed and the expression of MIP-2 mRNA in porcine pulmonary vascular macrophage (PIM) stimulated by lipopolysaccharide (LPS) was observed. The contents of tumor necrosis factor alpha (TNFα), interleukin- Changes, to explore the mechanism of lung injury. Results: The expression of MIP-2 and MCP-1 m RNA in the lungs of ALI rats increased significantly, reaching the peak at 3 h and 6 h (P <0.01), respectively. Plasma and lung homogenate myeloperoxidase (MPO) also increased significantly, but the peak value was lower; The expression of MIP-2 mRNA in lung tissue was positively correlated with MPO activity in plasma and lung homogenate (P <0-05). In situ hybridization showed that lung macrophages (M) are the major secretory cells of MIP-2. LPS-stimulated PIM secretion of TNFα early, IL-8 is late and long. Conclusion: Lung M may play an important role in the development of ALI through the secretion of MIP-2, TNFα, IL-8 and so on