ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2020
Sleep deprivation aggravated lipopolysaccharide/D-galactosamine-induced acute liver injury by suppressing melatonin production.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Melatonin: Roles and Molecular Mechanisms in Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomolecules · 2026Review
- Transcriptome-Based Revelation of the Effects of Sleep Deprivation on Hepatic Metabolic Rhythms in Tibetan Sheep (Animals : an open access journal from MDPI · 2024Article
- The protective effect of melatonin on chronic paradoxical sleep deprivation induced metabolic and memory deficit in rats.International journal of physiology, pathophysiology and pharmacology · 2023Article
- Exploration of the anti-insomnia mechanism of Ganoderma by central-peripheral multi-level interaction network analysis.BMC microbiology · 2021Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveSleep loss is common in patients with liver injury, but the effects of sleep deprivation (SD) on liver injury remain unclear. In the present study, the potential effects of SD on acute liver injury and the underlying mechanisms have been investigated.
methodsThe sleep of male BALB/c mice has been deprived by using a modified multiple platform water bath for 3 days and acute liver injury was induced by intraperitoneal injection of lipopolysaccharide (LPS) and D-galactosamine (D-Gal). The degree of liver injury was detected by aminotransferase determination, histopathology and survival rate analysis. Inflammatory response and melatonin (MT) were measured by enzyme-linked immunosorbent assay (ELISA). In addition, hepatocyte apoptosis was determined by caspase activity measurement and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay.
resultsWe observed that SD increased plasma aminotransferases, TUNEL-positive hepatocytes, histological abnormalities and mortality rates in mice with LPS/D-Gal treatment. SD also promoted LPS/D-Gal-induced production of TNF-α and upregulated hepatic caspase-8, caspase-9, and caspase-3 activities in LPS/D-Gal-exposed mice. In addition, SD significantly decreased MT contents in plasma of mice with acute liver injury, but supplementation with MT reversed these SD-promoted changes.
conclusionOur data suggested that SD exacerbated LPS/D-Gal-induced liver injury via decreasing melatonin production.
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