摘要
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。
AIM and METHOD: In order to identify the pathogenesis of acute lung injury (ALI), the expression of macrophage inflammatory protein-2(MIP-2), monocyte chemoattractant protein-1(MCP-1) was assessed in the rat lung tissue of endotoxin-induced ALI using dot and in situ hybridization technique. TNFα and IL-8 of supernatant from cultured LPS-treated pulmonary intravascular macrophage (PIM) were also measured. RESULTS:The expression of MIP-2, MCP-1 mRNA in ALI groups were markedly higher than control group ( P <0 01),and reaching their peaks at ALI 3 h and ALI 6 h group respectively. Level of MIP-2 mRNA positively related to the myeloperoxidase (MPO) activity in plasma and lung homogenate ( P <0 05). The positive signal of MIP-2 mRNA was localized in pulmonary macrophage (M ) and LPS-treated PIM. The release of TNF α in LPS-treated PIM occured earlier than that of IL-8; however, the level of IL-8 kept rising longer.CONCLUSION:Pulmonary M may play an important role in ALI by means of releasing MIP-2, TNF α,IL-8, etc.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第11期999-1002,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
