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Biosci Rep. 2019 Jan 8;39(1). pii: BSR20181215. doi: 10.1042/BSR20181215. Print 2019 Jan 31.

Metabolomics analysis of gut barrier dysfunction in a trauma-hemorrhagic shock rat model.

Author information

1
Department of Critical Care Medicine, Rizhao People's Hospital, Rizhao, Shandong, 276800, China.
2
Stroke Center, Rizhao Central Hospital, Rizhao, Shandong, 276800, China.
3
Department of Respiratory, Rizhao People's Hospital, Rizhao, Shandong, 276800, China.
4
Department of Vascular Interventional, Binzhou Medical University Hospital, Binzhou, Shandong, 256603, China Gangchen000@outlook.com.
5
Department of Respiratory, Yantai affiliated Hospital of Binzhou Medical University, Yantai, Shandong, 264100, China.
6
Department of Respiratory, Binzhou People's Hospital, Binzhou, Shandong, 256600, China.
7
Department of Critical Care Medicine, Affiliated Caner Hospital of Zhengzhou University and Henan Cancer Hospital, Zhengzhou, Henan, 450008, China.

Abstract

Intestinal barrier dysfunction has been implicated in the development of multiorgan dysfunction syndrome caused by the trauma-hemorrhagic shock (THS). However, the mechanisms underlying THS-induced gut barrier injury are still poorly understood. In the present study, we used the metabolomics analysis to test the hypothesis that altered metabolites might be related to the development of THS-induced barrier dysfunction in the large intestine. Under the induction of THS, gut barrier failure was characterized by injury of permeability and mucus layer, which were companied by the decreased expression of zonula occludens-1 in the colon and increased levels of inflammatory factors including tumor necrosis factor-α, interferon-γ, interleukin (IL)-6, and IL-1β in the serum. A total of 16 differential metabolites were identified in colonic tissues from THS-treated rats compared with control rats. These altered metabolites included dihydroxy acetone phosphate, ribose-5-phosphate, fructose, glyceric acid, succinic acid, and adenosine, which are critical intermediates or end products that are involved in pentose phosphate pathway, glycolysis, and tricarboxylic acid cycle as well as mitochondrial adenosine triphosphate biosynthesis. These findings may offer important insight into the metabolic alterations in THS-treated gut injury, which will be helpful for developing effective metabolites-based strategies to prevent THS-induced gut barrier dysfunction.

KEYWORDS:

Gut barrier; Metabolism; Metabolites; Metabolomics; Trauma-hemorrhagic shock

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