PMID- 15883743
OWN - NLM
STAT- MEDLINE
DCOM- 20050711
LR  - 20131121
IS  - 1023-3830 (Print)
IS  - 1023-3830 (Linking)
VI  - 54
IP  - 3
DP  - 2005 Mar
TI  - Insight into the involvement of Kupffer cell-derived mediators in the 
      hepatoprotective effect of glycine upon inflammation: study on rat precision-cut 
      liver slices.
PG  - 106-12
AB  - OBJECTIVE AND DESIGN: To investigate the role of inflammatory mediators in the 
      hepatoprotective effect of glycine against lipopolysaccharide (LPS)-induced liver 
      injury in rats. MATERIAL OR SUBJECTS: Male Wistar rats were used (N = 4 or 5 per 
      group). Precision-cut liver slices (PCLS) were prepared for in vitro studies. 
      TREATMENT: Glycine (10 mM) and LPS (10 mug/ml) were added to the incubation 
      medium of PCLS obtained 3 h after LPS intraperitoneal (i. p.) administration (10 
      mg/kg) or saline injection to rats. Glycine effects were also investigated in 
      vivo by treating rats with a diet containing glycine (5%) during 3 days. METHODS: 
      Tissue injury was assessed by measuring adenosine triphosphate (ATP) and glycogen 
      contents of liver tissue as well as by measuring aspartate aminotransferase 
      (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activity in 
      the medium (in vitro) or in the serum (in vivo). Tumor necrosis factor-alpha 
      (TNF-alpha), prostaglandin E(2)(PGE(2)) and NOx (reflecting nitric oxide 
      production) were measured in the incubation medium or in the serum. Histological 
      detection of both ED-2 and peroxidase activity were used as Kupffer cell markers. 
      Student t test or two-way ANOVA were used for statistic analysis. RESULTS: 
      Glycine added to the culture medium increased both ATP and glycogen contents of 
      PCLS from LPS-treated rats, reduced the production of TNF-alpha and NOx whereas 
      PGE(2) secretion by PCLS increased. In contrast to the in vitro effect of 
      glycine, we observed that a glycine-enriched diet decreased PGE(2) secretion in 
      the serum after LPS challenge. CONCLUSION: The effect of glycine on LPS-induced 
      mediator secretion is different considering in vitro or in vivo situations. 
      Interestingly, glycine in vitro is able to prevent energy status depletion of 
      PCLS occurring upon inflammation, a phenomenon probably linked to change in 
      inflammatory mediator secretion pattern by hepatic immune cells, namely Kupffer 
      cells.
FAU - Neyrinck, A M
AU  - Neyrinck AM
AD  - Unit of Pharmacokinetics, Metabolism, Nutrition and Toxicology, School of 
      Pharmacy, Universite Catholique de Louvain, 73 avenue Mounier, 1200 Brussels, 
      Belgium.
FAU - Margagliotti, S
AU  - Margagliotti S
FAU - Delzenne, N M
AU  - Delzenne NM
LA  - eng
PT  - Journal Article
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Culture Media)
RN  - 0 (Free Radicals)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 9005-79-2 (Glycogen)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 2.6.1.1 (Aspartate Aminotransferases)
RN  - EC 2.6.1.2 (Alanine Transaminase)
RN  - K7Q1JQR04M (Dinoprostone)
RN  - S88TT14065 (Oxygen)
RN  - TE7660XO1C (Glycine)
SB  - IM
MH  - Adenosine Triphosphate/chemistry
MH  - Alanine Transaminase/metabolism
MH  - Analysis of Variance
MH  - Animals
MH  - Aspartate Aminotransferases/metabolism
MH  - Culture Media/pharmacology
MH  - Dinoprostone/metabolism
MH  - Free Radicals/chemistry
MH  - Glycine/chemistry/*pharmacology
MH  - Glycogen/chemistry
MH  - Inflammation
MH  - Kupffer Cells/*metabolism
MH  - L-Lactate Dehydrogenase/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Liver/*drug effects/*metabolism
MH  - Male
MH  - Nitric Oxide/chemistry
MH  - Oxygen/chemistry
MH  - Rats
MH  - Rats, Wistar
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2005/05/11 09:00
MHDA- 2005/07/12 09:00
CRDT- 2005/05/11 09:00
PHST- 2005/05/11 09:00 [pubmed]
PHST- 2005/07/12 09:00 [medline]
PHST- 2005/05/11 09:00 [entrez]
AID - 10.1007/s00011-004-1330-9 [doi]
PST - ppublish
SO  - Inflamm Res. 2005 Mar;54(3):106-12. doi: 10.1007/s00011-004-1330-9.