PMID- 31966888
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200126
IS  - 1936-2625 (Electronic)
IS  - 1936-2625 (Linking)
VI  - 10
IP  - 9
DP  - 2017
TI  - Endoplasmic reticulum stress-mediated apoptosis signal pathway is involved in 
      sepsis-induced liver injury.
PG  - 9990-9997
AB  - Endoplasmic reticulum (ER) stress has been increasingly recognized to have an 
      important role in various liver diseases. Sepsis-induced multi-organ failure 
      remains to have a high mortality rate, and the liver plays a central 
      pathophysiological role. This study aims to explore whether ER stress is involved 
      in liver injury in septic rats. Sepsis was induced via cecal ligation and 
      puncture (CLP). Rats were randomly divided into five groups as follows: sham, CLP 
      2 h, CLP 6 h, CLP 12 h, and CLP 24 h. They were monitored to record body weight 
      (BW) and liver weight changes for every time point after surgery. The levels of 
      alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected 
      via colorimetric activity assays. In addition, the morphological changes of the 
      liver tissue were evaluated by staining the sections with hematoxylin and eosin 
      and observing under light microscopy. The levels of glucose-regulated protein 78 
      (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP), and cleaved 
      caspase-12 were detected via Western blot analysis. Apoptosis was detected via 
      terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) method. The 
      results showed that septic rat serums ALT and AST were increased, with the 
      increase being more obvious in the CLP 24 h group. In addition, septic rats 
      appeared to have histopathological abnormalities in the liver. The liver weight 
      and index increased after CLP. No differences were noted in the BW between septic 
      groups. The level of GRP78, CHOP, and cleaved caspase-12 were upregulated after 
      CLP. However, CHOP and caspase-12 were induced later than GRP78. The density of 
      TUNEL-positive apoptotic hepatocytes was significantly increased after 12 h and 
      24 h CLP. It indicates that the unfolded protein response occurred in the early 
      stage of sepsis-induced liver damage. The ER stress-mediated apoptosis signal 
      pathway is among the mechanisms of septic liver injury and may be a target in 
      clinical prevention and therapy of sepsis-induced liver injury.
CI  - IJCEP Copyright (c) 2017.
FAU - Qian, Wen-Juan
AU  - Qian WJ
AD  - Medical College of Shihezi University Shihezi, Xinjiang, China.
FAU - Cheng, Qing-Hong
AU  - Cheng QH
AD  - Department of Critical Care Medicine, First Affiliated Hospital of The Medical 
      College of Shihezi University Shihezi, Xinjiang, China.
LA  - eng
PT  - Journal Article
DEP - 20170901
PL  - United States
TA  - Int J Clin Exp Pathol
JT  - International journal of clinical and experimental pathology
JID - 101480565
PMC - PMC6965985
OTO - NOTNLM
OT  - Sepsis
OT  - apoptosis
OT  - caspase-12
OT  - endoplasmic reticulum stress
OT  - liver injury
COIS- None.
EDAT- 2017/09/01 00:00
MHDA- 2017/09/01 00:01
PMCR- 2017/09/01
CRDT- 2020/01/23 06:00
PHST- 2017/07/03 00:00 [received]
PHST- 2017/08/29 00:00 [accepted]
PHST- 2020/01/23 06:00 [entrez]
PHST- 2017/09/01 00:00 [pubmed]
PHST- 2017/09/01 00:01 [medline]
PHST- 2017/09/01 00:00 [pmc-release]
PST - epublish
SO  - Int J Clin Exp Pathol. 2017 Sep 1;10(9):9990-9997. eCollection 2017.