摘要
目的探讨巨噬细胞炎症蛋白-2(MIP-2)和细胞凋亡在小鼠内毒素诱导急性肺损伤发病机制中的作用。方法以脂多糖气管内注射建立小鼠急性肺损伤模型,进行肺组织病理、肺水含量、支气管肺泡灌洗液白细胞总数和中性粒细胞分类计数、TNF-α和MIP-2浓度检测,并作肺组织凋亡细胞计数。结果气管内注射LPS后,肺水含量、肺泡灌洗液白细胞总数和中性粒细胞分类计数、TNF-α和MIP-2浓度及肺组织凋亡细胞计数均明显升高,且随时间推移呈逐渐变化的趋势。结论MIP-2是炎症早期的促炎性细胞因子,其在早期短期急剧释放可趋化和激活中性粒细胞并诱导肺组织细胞凋亡,从而启动与维持炎症反应。
[Objective] To investigate the role of macrophage inflammatory protein （MIP） 2 and apoptosis in pathogenesis of murine acute lung injury induced by lipopolysaccharide. [Methods] The mouse model of acute lung injury was established via intratracheal instillation of lipopolysaccharide （LPS）, while the control groups was applied with saline. The mice were killed at 6 h, 12 h, 24 h after instillation of LPS or saline. Bronchoalveolar lavage fluid （BALF） and lung specimens were acquired. Total white cell count, differential count of neutrophil in BALF were detected. The concentration of TNF-α and MIP-2 in BALF was determined by ELISA. Ratio of wet to dry weight of lung tissues was also detected. The lung tissues were stainned by terminal-deoxynucleotidyl transferase mediated nick end labeling （TUNEL）, and counted numbers of apoptosis cells was acquired with image analysis software. [Results] Total white cell count, differential count of neutrophil, ratio of wet to dry weight, counted numbers of apoptosis cells and concentration of TNF-α and MIP-2 in BALF in LPS-indueed ALI of mice were increased compared with control groups （P 〈0.05, respectively）. [Conclusion] MIP-2 as a ehemokine for macrophage participates in acute lung injury induced by lipopolysaccharide. Apoptosis also make a critical role in it.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2007年第11期1304-1308,共5页
China Journal of Modern Medicine
基金
国家自然科学基金(No:30470761)
