PMID- 26915320
OWN - NLM
STAT- MEDLINE
DCOM- 20170501
LR  - 20181202
IS  - 0371-0874 (Print)
IS  - 0371-0874 (Linking)
VI  - 68
IP  - 1
DP  - 2016 Feb 25
TI  - [AMPK activator down-regulates the expression of tissue factor in fulminant 
      hepatitis mice].
PG  - 35-40
AB  - AMP activated protein kinase (AMPK) is a pivotal metabolic regulatory enzyme and 
      novel target of controlling inflammation. Our previous studies had demonstrated 
      that 5-amino-4-imidazolecarboxamide riboside (AICAR), an AMPK activator, 
      attenuated lipopolysaccharide (LPS)/D-galactosamine (D-gal)-induced fulminant 
      hepatitis via suppressing inflammatory response. Since inflammation usually 
      activates the coagulation response and aggravates inflammation-induced tissue 
      injury, the present study was to explore the effects of AICAR on 
      inflammation-induced activation of coagulation. Male BALB/c mice received 
      LPS/D-gal intraperitoneal injection were used as fulminant hepatitis model. 
      Western blot was used to detect tissue factor (TF) and hypoxia-inducible factor 
      1alpha (HIF-1alpha) protein expressions in hepatic tissue, as well as nuclear factor 
      kappa B (NF-kappaB) p65 translocation into the nucleus. Real-time quantitative PCR 
      was used to analyze erythropoietin (EPO) mRNA expression level. Lactic acid (LA) 
      level in hepatic tissue was detected by kit. The results showed that LPS/D-gal 
      induced the enhanced expression of TF, elevation of NF-kappaB p65 nuclear 
      translocation, up-regulation of HIF-1alpha and EPO expressions, and increased LA 
      level. These above alterations could be suppressed by AICAR. These results 
      suggest that AICAR may down-regulate LPS/D-gal-induced TF expression (coagulation 
      activity), and relieve hepatic hypoxia and metabolic disorder via suppressing the 
      activity of NF-kappaB, which may be a novel mechanism of the beneficial effect of 
      AICAR on LPS/D-gal-induced fulminant hepatitis.
FAU - Dai, Jie
AU  - Dai J
AD  - Hospital of Chongqing University of Arts and Sciences, Chongqing 402160, China.
FAU - Lin, Ling
AU  - Lin L
AD  - Department of Pathophysiology, Chongqing Medical University, Chongqing 400016, 
      China.
FAU - Zhou, Dan
AU  - Zhou D
AD  - Department of Pathophysiology, Chongqing Medical University, Chongqing 400016, 
      China.
FAU - Ai, Qing
AU  - Ai Q
AD  - Department of Physiology, Chongqing Medical University, Chongqing 400016, China.
FAU - Ge, Pu
AU  - Ge P
AD  - Department of Pathophysiology, Chongqing Medical University, Chongqing 400016, 
      China.
FAU - Zhang, Li
AU  - Zhang L
AD  - Department of Pathophysiology, Chongqing Medical University, Chongqing 400016, 
      China.
AD  - Laboratory of Stem Cell and Tissue Engineering, Chongqing Medical University, 
      Chongqing 400016, China. zhangli@cqmu.edu.cn.
LA  - chi
PT  - Journal Article
PL  - China
TA  - Sheng Li Xue Bao
JT  - Sheng li xue bao : [Acta physiologica Sinica]
JID - 20730130R
RN  - 0 (EPO protein, human)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 11096-26-7 (Erythropoietin)
RN  - 360-97-4 (Aminoimidazole Carboxamide)
RN  - 80658-49-7 (imidazolecarboxamide)
RN  - 9035-58-9 (Thromboplastin)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases
MH  - Aminoimidazole Carboxamide/analogs & derivatives
MH  - Animals
MH  - Down-Regulation
MH  - Erythropoietin
MH  - *Hepatitis
MH  - Hypoxia-Inducible Factor 1, alpha Subunit
MH  - Inflammation
MH  - Lipopolysaccharides
MH  - Male
MH  - Mice
MH  - NF-kappa B
MH  - Thromboplastin
MH  - Up-Regulation
EDAT- 2016/02/27 06:00
MHDA- 2017/05/02 06:00
CRDT- 2016/02/27 06:00
PHST- 2016/02/27 06:00 [entrez]
PHST- 2016/02/27 06:00 [pubmed]
PHST- 2017/05/02 06:00 [medline]
PST - ppublish
SO  - Sheng Li Xue Bao. 2016 Feb 25;68(1):35-40.