摘要
目的探讨细胞粘附因子-1(ICAM-1)与新生大鼠高氧肺损伤的关系以及高氧肺损伤的发病机制。方法取102只胎龄22天足月新生大鼠,随机分为实验组与对照组各51只。实验组生后立即置入持续高浓度氧(>95%)环境中饲养,对照组在空气中饲养。两组新生大鼠根据随机数字法于生后第3、7、14天各抽取8只定位相应亚组。处死新生鼠取其肺组织,HE染色观察肺组织病理变化,Masson三色染色判断肺组织纤维化程度,免疫组化检测ICAM-1并对表达强度进行半定量分析。结果 (1)对照组生后3、7、14天各亚组未见肺损伤的病理性改变,Masson三色染色未见胶原沉积增多现象,ICAM-1在肺组织中阴性或弱阳性表达。(2)实验组7天HE染色可见大量炎细胞浸润,肺间隔轻度增宽,14天炎细胞浸润减少,肺泡结构破坏较明显,肺间隔明显增厚;Masson三色染色生后7天胶原沉积开始增加,14天纤维化程度更加显著,ICAM-1在各时间点均呈阳性表达,且分布广泛;半定量分析显示,实验组各时间点ICAM-1的表达明显高于对照组,生后7天表达最强(P<0.05)。结论高氧对肺组织有明显的损害作用,高氧暴露早期ICAM-1在肺组织中的表达随着暴露时间的延长而增加,ICAM-1在高氧暴露早期的急性炎症阶段起作用,继续暴露则逐渐降低,并未证实其与高氧肺损伤后期的纤维化有关系。
Objective To explore the expression of intracellular adhesion molecule-1（ICAM-1） during hyperoxic lung injury and to investigate the pathological changes of hyperoxia related pulmonary injury.Methods A total of 102 full term neonatal sprague-dawley rats were randomized into experimental（hyperoxia） and control（room air） groups of 51 rats each.Newborn rats in the experimental group were kept in boxes that contain 95% oxygen immediately after deliveries,whereas those in the control group were raised in room air instead.Rats from both groups were further randomized,three subgroups of eight rats from each group were chosen and sacrificed on the 3,7 and the 14 days of life subsequently.Extracted lung tissue was HE stained to reveal the gross pathological changes;Masson Trichrome Stain was used to observe the severity of pulmonary fibrosis;Immunohistochemical Semi-quantitative analysis of ICAM-1 was then performed.Results（1） Rats in the control group have no pathological change of pulmonary tissue at 3,7 and 14 days of age and no increased expression of collagen on Masson stain.There was negative to weak positive pulmonary ICAM-1 expression in the control rats.（2） In contrary,the rats which were raised in the hyperoxia environment from birth have shown significant inflammatory cell infiltration.Mild thickening of alveoli septum were also found in pulmonary tissue by day 7 post partum.By day 14,inflammatory cell infiltration began to subsidize,however,more prominent alveoli structural damage and marked thickening of alveoli septum were found.On Masson stain,increased collagen deposits began to present by day seven,prominent fibrosis was found by day 14.ICAM-1 expression was widely present in all subgroups of the experimental rats at the 3rd,7th and the 14th day of life.Semi-quantitative analysis revealed that the pulmonary ICAM-expression in rats of all the experimental subgroups were marked higher than the level in the corresponding control subgroups,with the peak expression at day 7 of life（P0.05）.Conclusions High concentration oxygen exposure leads to prominent injury of lung tissue in neonatal rats.Shortly after birth,ICAM-1 expression elevates with increasing length of exposure to high concentration oxygen;however,ICAM-1 level gradually decreases with persistent usage of high concentration oxygen.Although the current study didn＇t reveal the correlation of ICAM-1 expression to hyperoxic pulmonary fibrosis,ICAM-1 is likely playing an active role in leukocyte adhesion to endothelium cells and in activation of cytokines during the acute inflammation phase of hyperoxic lung injury.
出处
《中国新生儿科杂志》
CAS
2012年第2期124-127,共4页
Chinese Journal of Neonatology
关键词
细胞粘附因子-1
高氧肺损伤
慢性肺疾病
Intercellular adhesion molecule-1
Hyperoxic lung injury
Chonic lung disease
