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Sleep deprivation aggravated lipopolysaccharide/ d -galactosamine-induced acute liver injury by suppressing melatonin production
Inflammation Research ( IF 6.7 ) Pub Date : 2020-08-18 , DOI: 10.1007/s00011-020-01393-3
Lu Liu , Li Zhang , Longjiang Li , Mengting Chen , Zhe Wang , Yi Shen , Jiayi Huang , Ling Tang

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.



中文翻译:

睡眠剥夺通过抑制褪黑激素的产生加重了脂多糖/ d-半乳糖胺诱导的急性肝损伤

目的

睡眠丧失在肝损伤患者中很常见,但是睡眠剥夺(SD)对肝损伤的影响仍不清楚。在本研究中,已经研究了SD对急性肝损伤的潜在作用及其潜在机制。

方法

使用改良的多平台水浴剥夺雄性BALB / c小鼠的睡眠3天,腹膜内注射脂多糖(LPS)和d-半乳糖胺(D-Gal)引起急性肝损伤。通过氨基转移酶测定,组织病理学和存活率分析来检测肝损伤的程度。通过酶联免疫吸附测定(ELISA)测定炎症反应和褪黑激素(MT)。另外,通过半胱天冬酶活性测量和末端脱氧核苷酸转移酶dUTP缺口末端标记(TUNEL)测定法测定肝细胞凋亡。

结果

我们观察到,用LPS / D-Gal治疗的小鼠,SD可增加血浆氨基转移酶,TUNEL阳性肝细胞,组织学异常和死亡率。SD还促进了LPS / D-Gal暴露的小鼠中LPS / D-Gal诱导的TNF-α的产生,并上调了肝caspase-8,caspase-9和caspase-3的活性。此外,SD可显着降低急性肝损伤小鼠血浆中MT含量,但补充MT可逆转这些SD促进的变化。

结论

我们的数据表明,SD通过降低褪黑激素的产生加剧了LPS / D-Gal诱导的肝损伤。

更新日期:2020-09-28
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