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内毒素诱导急性肺损伤巨噬细胞炎症蛋白-2的表达 被引量:2

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摘要 目的:探讨趋化性细胞因子巨噬细胞炎症蛋白-2(MIP-2)在内毒素诱导急性肺损伤(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MIP-2mRNA的表达进行定量和定位研究。结果:内毒素性ALI各组大鼠肺组织MIP-2mRNA表达量显著高于对照组,且在峰值水平与血浆及肺组织匀浆髓过氧化物酶(MPO)活力呈正相关(r=0.729,r=0.885,P<0.05)。原位杂交发现在ALI早期肺内巨噬细胞是MIP-2的主要分泌细胞。结论:肺巨噬细胞释放的MIP-2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,因而参与了ALI的早期发病过程。 Objective: To study the potential role of chemotactic macrophage inflammatory protein 2 (MIP 2) in the development of LPS induced acute lung injury (ALI). Methods: The amount and distribution of MIP 2 were determined in the lungs with ALI. Results: The expression of MIP 2 mRNA was significantly higher in the lungs of the animals with ALI than those of the control ( P <0.01). In addition, The expression level of MIP 2 mRNA was positively correlated to the activity of myeloperoxidase in the plasma and lung homogenate ( r =0.729, r =0.885 and P <0.05). It was confirmed with in situ hybridization that pulmonary macrophages were the predominant source of MIP 2 in the early stage of ALI. Conclusion: MIP 2 released mainly from pulmonary macrophages might contribute to the activation and sequestration of polymorphonuclear leucocytes in the lungs challenged with LPS. So MIP 2 might take part in the development of LPS induced ALI.
出处 《第三军医大学学报》 CAS CSCD 北大核心 1999年第4期235-237,共3页 Journal of Third Military Medical University
基金 国家自然科学基金
关键词 巨噬细胞 炎症蛋白-2 急性 肺损伤 内毒素 macrophage inflammatory protein 2 endotoxin acute lung injury
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