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饮食诱导的小鼠肺部炎症和早期纤维化:中性粒细胞炎症的可能作用。

Diet-Induced Pulmonary Inflammation and Incipient Fibrosis in Mice: a Possible Role of Neutrophilic Inflammation.

机构信息

Laboratory of Experimental and Translational Medicine, Multidisciplinary Institute of Biological Research-San Luis, IMIBIO-SL, CONICET, National University of San Luis, Suite 13X, First Floor, Chacabuco 917, 5700, San Luis, San Luis, Argentina.

Laboratory of Experimental Therapeutics and Nutrition, IMIBIO-SL, CONICET, National University of San Luis, 5700, San Luis, San Luis, Argentina.

出版信息

Inflammation. 2019 Oct;42(5):1886-1900. doi: 10.1007/s10753-019-01051-9.

DOI:10.1007/s10753-019-01051-9
PMID:31359324
Abstract

Chicken fat and fructose are added into food-processing to reduce costs and enhance acceptability; however, these additives turn food into unhealthy and hypercaloric meals. Herein we have hypothesized that chronic feeding with chicken fat and fructose, together or by separate, can cause pulmonary redox and inflammatory changes. These changes are particularly related to neutrophils and myeloperoxidase, with consequent changes in the organ histophysiology. To test this hypothesis, we fed mice for 16 weeks with either control food (low-fat diet, LFD) or control food supplemented with 22% chicken fat and with or without 10% fructose in the drinking water. At the end of the feeding regimen, we measured redox and inflammatory changes in the lung with particular emphasis on neutrophil accumulation/activation and molecular-histological markers of fibrosis. Our results suggest that a diet supplemented with chicken fat and fructose causes additive effects on pulmonary oxidative stress, inflammation, and a pro-fibrotic status. Neutrophilic inflammation may play a critical role in pulmonary pathology associated with metabolic syndrome.

摘要

在食品加工中添加鸡油和果糖以降低成本并提高可接受性;然而,这些添加剂会使食物变成不健康和高热量的餐食。在此,我们假设长期食用鸡油和果糖,无论是单独食用还是一起食用,都会导致肺部氧化还原和炎症变化。这些变化与中性粒细胞和髓过氧化物酶特别相关,从而导致器官组织生理学发生变化。为了验证这一假设,我们用控制饮食(低脂饮食,LFD)或添加 22%鸡油的控制饮食喂养小鼠 16 周,并在饮用水中添加或不添加 10%果糖。在喂养方案结束时,我们测量了肺中的氧化还原和炎症变化,特别强调中性粒细胞的积累/激活以及纤维化的分子组织学标志物。我们的结果表明,添加鸡油和果糖的饮食对肺部氧化应激、炎症和促纤维化状态有相加作用。中性粒细胞炎症可能在与代谢综合征相关的肺部病理中起关键作用。

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本文引用的文献

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A Mouse Model of Diet-Induced Obesity Resembling Most Features of Human Metabolic Syndrome.一种类似于人类代谢综合征大多数特征的饮食诱导肥胖小鼠模型。
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[Tumor necrosis factor-α inhibitor protects against myocardial ischemia/reperfusion injury via Notch1 mediated inhibition of oxidative/nitrative stress in traumatic mice].
肺纤维化与糖尿病:同一枚硬币的两面。
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Inflammasome activation and metabolic remodelling in p16-positive aging cells aggravates high-fat diet-induced lung fibrosis by inhibiting NEDD4L-mediated K48-polyubiquitin-dependent degradation of SGK1.p16 阳性衰老细胞中炎性小体的激活和代谢重塑通过抑制 NEDD4L 介导的 SGK1 的 K48-多聚泛素依赖性降解加重高脂肪饮食诱导的肺纤维化。
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