首页> 外文期刊>Scandinavian journal of clinical and laboratory investigation. >Dynamic investigation of alveolar type II cell function in a long-term survival model of rat lung ischemia-reperfusion injury.
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Dynamic investigation of alveolar type II cell function in a long-term survival model of rat lung ischemia-reperfusion injury.

机译:大鼠肺缺血再灌注损伤长期生存模型中肺泡II型细胞功能的动态研究。

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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.
机译:背景:II型肺泡(ATII)细胞能够修复由肺缺血再灌注损伤(LIRI)引起的肺泡上皮损伤。在本研究中,我们旨在使用大鼠LIRI的长期存活模型动态研究ATII细胞的形态和功能改变。材料与方法:将雄性Sprague-Dawley大鼠随机分为假手术组和缺血再灌注(IR)组。 IR组的动物通过左肺门闭塞进行热缺血60分钟。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价ATII细胞的增殖概况。通过逆转录聚合酶链反应确定表面活性剂蛋白C(SP-C)和caspase-3的表达。超微结构和立体分析用于量化ATII细胞的核和层状体(LBs)的变化。结果:与假手术组相比,IR组SP-C表达在LIRI早期明显下降,并在再灌注后7天恢复正常。 SP-C / PCNA双阳性细胞数在1d时明显增加,在3d时达到峰值,并在再灌注后第7天降至正常。 ATII细胞的超微结构和立体分析还显示,LBs在LIRI的早期显着受损,并在再灌注后长达7天恢复。结论:该模型简单,稳定且可重现。在LIRI早期之后,ATII细胞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愈LIRI的潜在方法。

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