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Role of angiotensin-converting enzyme (ACE) and ACE2 in a rat model of smoke inhalation induced acute respiratory distress syndrome

机译:血管紧张素转换酶(ACE)和ACE2在烟吸入引起的急性呼吸窘迫综合征大鼠模型中的作用

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Smoke inhalation induced acute respiratory distress syndrome (ARDS) has become more and more common throughout the world and it is hard to improve the outcome. The present research was to investigate possible roles of angiotensin-converting enzyme (ACE) and ACE2 in lung injury resulted from smoke exposure. Rats were exposed to dense smoke to induce ARDS. Histological changes, blood gases, bronchoalveolar lavage fluids (BALF) and wet-to-dry weight were analyzed to evaluate lung injury after smoke inhalation; beside, we also measured the expression of ACE and ACE2 at different time points to explore the possible mechanism of those changes. The results showed that pH of arterial blood, partial blood oxygen (PaO2) and blood oxygen saturation (SO2) decreased after smoke inhalation at different time points (P < 0.01); while, partial blood carbon dioxide (PaCO2), wet-to-dry weight ratio, leukocytes count, protein concentration and inflammatory cytokines in BALF increased after smoke exposure (P < 0.01). More importantly, both immunohistochemical staining and Western blot results showed that ACE and ACE2 expression in lungs from the experimental groups significantly increased compared with that of the control group (P < 0.05). This study indicated that inflammation pulmonary edema and histological changes resulted from smoke inhalation induced lung injury were possibly attributed to abnormal expression of ACE and ACE2 related pathway. (C) 2015 Elsevier Ltd and ISBI. All rights reserved.
机译:烟雾吸入引起的急性呼吸窘迫综合征(ARDS)在世界范围内变得越来越普遍,很难改善结果。本研究旨在调查血管紧张素转换酶(ACE)和ACE2在烟雾暴露引起的肺损伤中的可能作用。大鼠暴露于浓烟中诱发ARDS。分析组织学变化,血气,支气管肺泡灌洗液(BALF)和干重至干重,以评估吸入烟后的肺损伤。此外,我们还测量了ACE和ACE2在不同时间点的表达,以探讨这些变化的可能机制。结果表明,在不同时间点吸入烟气后,动脉血的pH,部分血氧(PaO2)和血氧饱和度(SO2)降低(P <0.01)。烟暴露后,BALF中的部分血液二氧化碳(PaCO2),干重比,白细胞计数,蛋白质浓度和炎性细胞因子增加(P <0.01)。更重要的是,免疫组织化学染色和蛋白质印迹结果均显示,与对照组相比,实验组肺中的ACE和ACE2表达显着增加(P <0.05)。这项研究表明,烟雾吸入引起的肺损伤引起的炎症性肺水肿和组织学改变可能归因于ACE和ACE2相关通路的异常表达。 (C)2015 Elsevier Ltd和ISBI。版权所有。

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