论文部分内容阅读
目的:研究信号转导因子与转录活化因子(STAT)在高氧肺损伤中的表达及STAT对高氧肺损伤气道炎症调控,以探讨STAT信号传导在高氧肺损伤发病机制中的作用。方法:48只大鼠分为空气组1,3,7,14天组,高氧组1,3,7,14天组,光镜下观察各组病理变化,观察高氧环境下羟脯氨酸含量变化和肺组织巨噬细胞的变化,免疫组化方法检测STAT及细胞粘附因子-1(ICAM-1)的表达。结果:高氧组的羟脯氨酸含量在3,7,14天组均明显高于对照组;支气管肺泡灌洗中巨噬细胞明显升高。对照组及高氧组STAT积分吸光度在第1天(11.2±2.1 vs 19.4±4.2),第3天(9.8±3.4 vs 39.8±3.9),第7天(10.6±2.8 vs 63.5±6.2),第14天(12.3±2.9 vs 30.5±4.9),两组对比均有统计学差异;对照组及高氧组ICAM-1积分吸光度,除第1天外,两组对比均有统计学差异。结论:高氧肺损伤后羟脯氨酸含量明显升高,出现巨噬细胞浸润,提示有肺纤维化趋势及炎症因子的作用,同时STAT持续活化及过度表达,主要表达于气道上皮细胞及巨噬细胞,ICAM-1持续表达,提示STAT与高氧肺损伤的炎症反应有关,在高氧肺损伤炎症调控中起重要作用。
OBJECTIVE: To investigate the expression of signal transducer and activator of transcription (STAT) in hyperoxic lung injury and the regulation of STAT on airway inflammation in hyperoxia-induced lung injury in order to investigate the role of STAT signaling in the pathogenesis of hyperoxic lung injury. Methods: Forty-eight rats were divided into 1, 3, 7, and 14 days in the air group and 1, 3, 7 and 14 days in the aerobic group. The pathological changes were observed under light microscope. Acid content and the changes of macrophages in lung tissue. The expressions of STAT and cell adhesion molecule-1 (ICAM-1) were detected by immunohistochemistry. Results: The levels of hydroxyproline in hyperoxia group were significantly higher than those in control group on days 3, 7 and 14; macrophages in bronchoalveolar lavage significantly increased. The absorbance of STAT in control group and hyperoxia group was significantly higher than that of control group (P <0.01) 14 days (12.3 ± 2.9 vs 30.5 ± 4.9). The ICAM-1 integral absorbance of control group and hyperoxia group were statistically different except Day 1. CONCLUSION: Hypoxic lung injury significantly increases the content of hydroxyproline and macrophage infiltration, which indicates the tendency of pulmonary fibrosis and inflammatory cytokines. Meanwhile, STAT continues to be activated and overexpressed, which is mainly expressed in airway epithelial cells and Macrophages, ICAM-1 sustained expression, suggesting that STAT and hyperoxia lung injury in the inflammatory response, play an important role in the regulation of inflammation in hyperoxia-induced lung injury.