Angiotensin-(1-7) inhibits inflammation and oxidative stress to relieve lung injury induced by chronic intermittent hypoxia in rats.
Angiotensin-(1-7) inhibits inflammation and oxidative stress to relieve lung injury induced by chronic intermittent hypoxia in rats.
复制标题
血管紧张素-(1-7)抑制炎症和氧化应激减轻大鼠慢性间歇性缺氧所致肺损伤
DOI：
10.1590/1414-431x20165431
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发表时间：
2016-09-01
期刊：
影响因子：
--
通讯作者：
Xu L
中科院分区：
文献类型：
--
作者：
Lu W;Kang J;Hu K;Tang S;Zhou X;Yu S;Li Y;Xu L
阻塞性睡眠呼吸暂停与肺组织中的炎症和氧化应激有关，并可导致代谢异常。本实验观察了血管紧张素1 -7 [Ang-（1-7）]对慢性间歇性缺氧（CIH）所致大鼠肺损伤的影响。我们将32只雄性Sprague-Dawley大鼠（180-200 g）随机分为常氧对照组（NC）、CIH未治疗组（uCIH）、Ang-（1-7）治疗常氧对照组（N-A）和Ang-（1-7）治疗CIH组（CIH-A）。测定肺组织中的氧化应激生物标志物，并通过Western blot和逆转录聚合酶链反应测定NADPH氧化酶4（Nox 4）和Nox亚基（p22 phox和p47 phox）的表达。uCIH组肺组织病理改变较其他各组明显。酶联免疫吸附试验和免疫组化染色显示，uCIH组血清和肺组织中炎性因子浓度均显著高于NC组和N-A组。CIH-A组炎性因子表达明显高于NC组和N-A组，但低于uCIH组（P<0.01）。uCIH组的氧化应激水平明显高于NC组和N-A组。uCIH组Nox 4及其亚单位的表达也增加。这些变化在Ang-（1-7）处理后减弱。总之，用Ang-（1-7）治疗通过抑制炎症和氧化应激逆转CIH诱导的肺损伤的体征。
Obstructive sleep apnea is associated with inflammation and oxidative stress in lung tissues and can lead to metabolic abnormalities. We investigated the effects of angiotensin1–7 [Ang-(1–7)] on lung injury in rats induced by chronic intermittent hypoxia (CIH). We randomly assigned 32 male Sprague-Dawley rats (180–200 g) to normoxia control (NC), CIH-untreated (uCIH), Ang-(1–7)-treated normoxia control (N-A), and Ang-(1–7)-treated CIH (CIH-A) groups. Oxidative stress biomarkers were measured in lung tissues, and expression of NADPH oxidase 4 (Nox4) and Nox subunits (p22phox, and p47phox) was determined by Western blot and reverse transcription-polymerase chain reaction. Pulmonary pathological changes were more evident in the uCIH group than in the other groups. Enzyme-linked immunosorbent assays and immunohistochemical staining showed that inflammatory factor concentrations in serum and lung tissues in the uCIH group were significantly higher than those in the NC and N-A groups. Expression of inflammatory factors was significantly higher in the CIH-A group than in the NC and N-A groups, but was lower than in the uCIH group (P<0.01). Oxidative stress was markedly higher in the uCIH group than in the NC and N-A groups. Expression of Nox4 and its subunits was also increased in the uCIH group. These changes were attenuated upon Ang-(1–7) treatment. In summary, treatment with Ang-(1-7) reversed signs of CIH-induced lung injury via inhibition of inflammation and oxidative stress.