Short-term glutamine supplementation decreases lung inflammation and the receptor for advanced glycation end-products expression in direct acute lung injury in mice

doi:10.1186/1471-2466-14-115

CNU IR > Pharmacy and Science > Dept. of Health and Nutrition (including master's program) > Periodical Articles > Item 310902800/28695

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Title:	Short-term glutamine supplementation decreases lung inflammation and the receptor for advanced glycation end-products expression in direct acute lung injury in mice
Authors:	Chuang, Yin-Ching Shaw, Huey-Mei Chen, Chi-Chung Pan, He-Jia Lai, Wei-Chih Huang, Hui-Ling
Contributors:	保健營養系
Keywords:	Glutamine (GLN) Acute lung injury (ALI) Receptor for advanced glycation end-products (RAGE) Inflammation
Date:	2014-07
Issue Date:	2015-05-06 21:25:27 (UTC+8)
Publisher:	Biomed Central Ltd
Abstract:	Background: Glutamine (GLN) has been reported to improve clinical and experimental sepsis outcomes. However, the mechanisms underlying the actions of GLN remain unclear, and may depend upon the route of GLN administration and the model of acute lung injury (ALI) used. The aim of this study was to investigate whether short-term GLN supplementation had an ameliorative effect on the inflammation induced by direct acid and lipopolysaccharide (LPS) challenge in mice. Methods: Female BALB/c mice were divided into two groups, a control group and a GLN group (4.17% GLN supplementation). After a 10-day feeding period, ALI was induced by intratracheal administration of hydrochloric acid (pH 1.0; 2 mL/kg of body weight [BW]) and LPS (5 mg/kg BW). Mice were sacrificed 3 h after ALI challenge. In this early phase of ALI, serum, lungs, and bronchoalveolar lavage fluid (BALF) from the mice were collected for further analysis. Results: The results of this study showed that ALI-challenged mice had a significant increase in myeloperoxidase activity and expression of interleukin (IL)-1 beta, IL-6, and tumor necrosis factor-alpha in the lung compared with unchallenged mice. Compared with the control group, GLN pretreatment in ALI-challenged mice reduced the levels of receptor for advanced glycation end-products (RAGE) and IL-1 beta production in BALF, with a corresponding decrease in their mRNA expression. The GLN group also had markedly lower in mRNA expression of cyclooxygenase-2 and NADPH oxidase-1. Conclusions: These results suggest that the benefit of dietary GLN may be partly contributed to an inhibitory effect on RAGE expression and pro-inflammatory cytokines production at an early stage in direct acid and LPS-induced ALI in mice.
Relation:	Bmc Pulmonary Medicine, v.14, pp.115
Appears in Collections:	[Dept. of Health and Nutrition (including master's program)] Periodical Articles

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