Sleep deprivation aggravated lipopolysaccharide/ d -galactosamine-induced acute liver injury by suppressing melatonin pr
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Inflammation Research
ORIGINAL RESEARCH PAPER
Sleep deprivation aggravated lipopolysaccharide/d‑galactosamine‑induced acute liver injury by suppressing melatonin production Lu Liu1 · Li Zhang2 · Longjiang Li2 · Mengting Chen3 · Zhe Wang4 · Yi Shen2 · Jiayi Huang2 · Ling Tang4 Received: 20 February 2020 / Revised: 13 July 2020 / Accepted: 11 August 2020 © Springer Nature Switzerland AG 2020
Abstract Objective Sleep 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. Methods The 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. Results We 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. Conclusion Our data suggested that SD exacerbated LPS/D-Gal-induced liver injury via decreasing melatonin production. Keywords SD · Liver injury · Inflammation · Apoptosis · MT
Introduction
Communicated by John Di Battista. Lu Liu and Li Zhang contributed equally to this work. * Ling Tang [email protected] 1
2
Department of Rehabilitation Medicine and Physical Therapy, The Affiliated Rehabilitation Hospital of Chongqing Medical University, 50 Xiejiawan Cultural Seventh Village, Jiulongpo District, Chongqing 400050, China Department of Pathophysiology, Chongqing Medical University, 1 Yixueyuan Road, Chongqing 400016, China
Acute liver injury, generally caused by drug abuse, viral infection, heavy drinking, etc., is a severe clinical syndrome that leads to liver failure and even death [1]. The uncontrolled inflammatory response has been regarded as a prominent mechanism that underlies the development of acute liver injury [2, 3]. Interestingly, patients with severe 3
Department of Neurology, The Affiliated Rehabilitation Hospital of Chongqing Medical University, 50 Xiejiawan Cultural Seventh Village, Jiulongpo District, Chongqing 400050, China
4
Department of Neurology, University-Town Hospital of Chongqing Medical University, 55 Middle Road, Univer
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