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首页> 外文期刊>Journal of Cachexia, Sarcopenia and Muscle >Inflammation, organomegaly, and muscle wasting despite hyperphagia in a mouse model of burn cachexia
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Inflammation, organomegaly, and muscle wasting despite hyperphagia in a mouse model of burn cachexia

机译：尽管有食欲亢进，在烧伤恶病质的小鼠模型中炎症，器官肥大和肌肉消瘦

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BackgroundBurn injury results in a chronic inflammatory, hypermetabolic, and hypercatabolic state persisting long after initial injury and wound healing. Burn survivors experience a profound and prolonged loss of lean body mass, fat mass, and bone mineral density, associated with significant morbidity and reduced quality of life. Understanding the mechanisms responsible is essential for developing therapies. A complete characterization of the pathophysiology of burn cachexia in a reproducible mouse model was lacking.MethodsYoung adult (12–16?weeks of age) male C57BL/6J mice were given full thickness burns using heated brass plates or sham injury. Food and water intake, organ and muscle weights, and muscle fiber diameters were measured. Body composition was determined by Piximus. Plasma analyte levels were determined by bead array assay.ResultsSurvival and weight loss were dependent upon burn size. The body weight nadir in burned mice was 14?days, at which time we observed reductions in total body mass, lean carcass mass, individual muscle weights, and muscle fiber cross-sectional area. Muscle loss was associated with increased expression of the muscle ubiquitin ligase, MuRF1. Burned mice also exhibited reduced fat mass and bone mineral density, concomitant with increased liver, spleen, and heart mass. Recovery of initial body weight occurred at 35?days; however, burned mice exhibited hyperphagia and polydipsia out to 80?days. Burned mice had significant increases in serum cytokine, chemokine, and acute phase proteins, consistent with findings in human burn subjects.ConclusionsThis study describes a mouse model that largely mimics human pathophysiology following severe burn injury. These baseline data provide a framework for mouse-based pharmacological and genetic investigation of burn-injury-associated cachexia.
机译：背景烧伤会导致慢性炎症，高代谢和高分解代谢状态，这种状态在初次受伤和伤口愈合后很长时间持续存在。烧伤幸存者经历了长期，长期的瘦体重，脂肪和骨矿物质密度损失，这与明显的发病率和生活质量下降有关。了解负责任的机制对于开发疗法至关重要。尚缺乏可再现的小鼠模型中烧伤恶病质的病理生理特征。方法：使用加热的黄铜板或假手术将年轻成年（12-16周龄）雄性C57BL / 6J小鼠完全烧伤。测量食物和水的摄入量，器官和肌肉的重量以及肌肉纤维的直径。身体成分由Piximus确定。通过磁珠阵列测定法测定血浆分析物水平。结果生存和体重减轻取决于烧伤大小。烧伤小鼠的体重最低点为14天​​，这时我们观察到总体重，瘦lean体体重，单个肌肉重量和肌肉纤维横截面积的减少。肌肉丢失与肌肉泛素连接酶MuRF1的表达增加有关。烧伤的小鼠还表现出脂肪量和骨矿物质密度降低，并伴有肝脏，脾脏和心脏质量的增加。最初的体重在35天时恢复。然而，烧伤的小鼠在长达80天的时间内表现出食欲亢进和烦躁不安。烧伤的小鼠血清细胞因子，趋化因子和急性期蛋白显着增加，与人类烧伤受试者的发现一致。结论本研究描述了一种小鼠模型，该模型在很大程度上模拟了严重烧伤后的人体病理生理。这些基线数据为烧伤相关恶病质的基于鼠标的药理和遗传研究提供了框架。

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