高氧所致小鼠急性肺损伤时一氧化氮合成酶的表达

目的探讨一氧化氮合成酶(INOS,eNOS)在高氧所致急性肺损伤发病过程中的作用.方法将54只小鼠置于密闭的氧气室暴露于＞95%的高氧,另18只小鼠呼吸正常空气作为对照组;分别于24、48 h和72 h取出小鼠,评价肺损伤程度同时进行支气管肺泡灌洗液细胞分类和计数;免疫组织化学测定肺组织iNOS和eNOS的表达及组织分布.结果高氧能引起急性肺损伤伴支气管肺汽灌洗液细胞总数、巨噬细胞、中性粒细胞数均明显增加;免疫组织化学研究显示iNOS和eNOS蛋白主要表达于气道上皮细胞、血管平滑肌细胞和巨噬细胞的胞浆中,它们在气道上皮细胞的表达在高氧环境下明显升高.结论在高氧环境下一氧化氮合成酶通过促进肺组织中一氧化氮合成从而在高氧所致的急性肺损伤过程中发挥重要作用.

Expression of nitric oxide synthase in mice with hyperoxia-induced acute lung injury

Objective To investigate the role of nitric oxide synthase (NOS) in the pathogenesis of acute lung injury induced by hyperoxia. Methods Seventy-two mice were exposed to oxygen (for 24 to 72 h) in sealed cages >95%, the severity of lung injury was evaluated, the expression of iNOS and eNOS in lung tissue at 24,48 and 72 hours of hyperoxia were studied by immunohistochemistry (IHC). Results Acute lung injury was caused hyperoxia, accompanied by increased total cell, macrophage and neutrophil counts in BALF. IHC study showed iNOS and eNOS protein were mainly localized in the cytoplasm of airway epithelial cells, alveolar macrophages and vascular smooth muscle cells. The expression of iNOS and eNOS protein in airway epithelium increased greatly in hyperoxia-induced lung injury. Conclusion NOS played an important role in the development of hyperoxia-induced lung injury in mice lung.