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在大鼠肺缺血再灌注损伤的长期生存模型中对肺泡 II 型细胞功能的动态研究。

Dynamic investigation of alveolar type II cell function in a long-term survival model of rat lung ischemia-reperfusion injury.

机构信息

Department of Thoracic Surgery, Nanjing Medical University Affiliated Cancer Hospital of Jiangsu Province, Cancer Institution of Jiangsu Province, Nanjing, P. R. China.

出版信息

Scand J Clin Lab Invest. 2010 Sep;70(5):364-73. doi: 10.3109/00365513.2010.495415.

DOI:10.3109/00365513.2010.495415
PMID:20560845
Abstract

BACKGROUND

Alveolar type II (ATII) cells are capable of repairing the alveolar epithelium injury induced by lung ischemia-reperfusion injury (LIRI). In the present study, we aim to dynamically investigate the morphological and functional alternations of ATII cells using a long-term survival model of rat LIRI.

MATERIALS AND METHODS

Male Sprague-Dawley rats were randomized into sham and ischemia-reperfusion (IR) groups. Animals of IR group underwent warm ischemia for 60 minutes by left pulmonary hilum occlusion. Injury was assessed by histological examination and myeloperoxidase activity assay. The proliferation profile of ATII cells was evaluated by immunofluorescence double staining. Surfactant protein-C (SP-C) and caspase-3 expression were determined by reverse transcription polymerase chain reaction. Ultrastructure and stereological analysis were used to quantify the alterations of nuclei and lamellar bodies (LBs) of ATII cells.

RESULTS

As compared with the sham group, SP-C expression in the IR group significantly decreased at the early phase of LIRI and returned to normal in 7 days after reperfusion. SP-C/PCNA double positive cell number significantly increased at 1d, peaked at 3d and decreased to normal until 7 days after reperfusion. Ultrastructure and stereological analysis of ATII cells also showed that LBs were remarkably impaired at the early phase of LIRI and recovered up to 7 days after reperfusion.

CONCLUSIONS

This model is simple, stable and reproducible. ATII cells demonstrated a self-repair capacity in a slow manner following the early phase of LIRI. Enhancing self-repair capacity of ATII cells may be a potential way of alleviating or curing LIRI.

摘要

背景

肺泡 II 型(ATII)细胞能够修复肺缺血再灌注损伤(LIRI)引起的肺泡上皮损伤。本研究旨在通过大鼠 LIRI 的长期存活模型,动态研究 ATII 细胞的形态和功能变化。

材料和方法

雄性 Sprague-Dawley 大鼠随机分为假手术和缺血再灌注(IR)组。IR 组动物通过左肺门阻断进行 60 分钟的热缺血。通过组织学检查和髓过氧化物酶活性测定评估损伤。通过免疫荧光双重染色评估 ATII 细胞的增殖情况。通过逆转录聚合酶链反应测定表面活性蛋白-C(SP-C)和半胱天冬酶-3 的表达。使用超微结构和体视学分析来定量 ATII 细胞细胞核和板层小体(LB)的变化。

结果

与假手术组相比,IR 组 SP-C 表达在 LIRI 的早期阶段显著降低,再灌注 7 天后恢复正常。SP-C/PCNA 双阳性细胞数在 1d 时显著增加,在 3d 时达到峰值,并在再灌注 7 天后恢复正常。ATII 细胞的超微结构和体视学分析也表明,在 LIRI 的早期阶段,LB 明显受损,并在再灌注 7 天后恢复。

结论

该模型简单、稳定、可重复。ATII 细胞在 LIRI 的早期阶段以缓慢的方式表现出自我修复能力。增强 ATII 细胞的自我修复能力可能是缓解或治疗 LIRI 的一种潜在方法。

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