ArticleBioscience reports2019
Metabolomics analysis of gut barrier dysfunction in a trauma-hemorrhagic shock rat model.
Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Metabolomics after trauma in experimental models- a systematic review.Langenbeck's archives of surgery · 2026Pooled it
- Arterial compliance is improved via enteral serine protease inhibition in experimental trauma/hemorrhagic shock.Frontiers in physiology · 2025Article
- POSTINJURY PNEUMONIA INDUCES A UNIQUE BLOOD MICROBIOME SIGNATURE.Shock (Augusta, Ga.) · 2024Article
- Lizhong Decoction Ameliorates Ulcerative Colitis in Mice via Regulation of Plasma and Urine Metabolic Profiling.Chinese journal of integrative medicine · 2022Article
- Enteral gabexate mesilate improves volume requirements and autonomic cardiovascular function after experimental trauma/hemorrhagic shock in the absence of blood reperfusion.American journal of translational research · 2022Article
- Long-Term Cardiac Damage Associated With Abdominal Irradiation in Mice.Frontiers in pharmacology · 2022Article
- Recent Developments in Mouse Trauma Research Models: A Mini-Review.Frontiers in physiology · 2022Review
- Diallyl Disulfide (DADS) Ameliorates IntestinalFrontiers in cellular and infection microbiology · 2021Article
- Lizhong decoction ameliorates ulcerative colitis in mice via modulating gut microbiota and its metabolites.Applied microbiology and biotechnology · 2020Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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