PMID- 19144177
OWN - NLM
STAT- MEDLINE
DCOM- 20090505
LR  - 20240416
IS  - 1471-230X (Electronic)
IS  - 1471-230X (Linking)
VI  - 9
DP  - 2009 Jan 14
TI  - Paraoxonase-1 is related to inflammation, fibrosis and PPAR delta in experimental 
      liver disease.
PG  - 3
LID - 10.1186/1471-230X-9-3 [doi]
AB  - BACKGROUND: Paraoxonase-1 (PON1) is an antioxidant enzyme synthesized by the 
      liver. It protects against liver impairment and attenuates the production of the 
      pro-inflammatory monocyte chemoattractant protein-1 (MCP-1). We investigated the 
      relationships between hepatic PON1 and MCP-1 expression in rats with liver 
      disease and explored the possible molecular mechanisms involved. METHODS: CCl4 
      was administered for up to 12 weeks to induce liver damage. Serum and hepatic 
      levels of PON1 and MCP-1, their gene and protein expression, nuclear 
      transcription factors, and histological and biochemical markers of liver 
      impairment were measured. RESULTS: High levels of PON1 and MCP-1 expression were 
      observed at 12th week in the hepatocytes surrounding the fibrous septa and 
      inflammatory areas. CCl4-administered rats had an increased hepatic PON1 
      concentration that was related to decreased gene transcription and inhibited 
      protein degradation. Decreased PON1 gene transcription was associated with 
      PPARdelta expression. These changes were accompanied by increased hepatic MCP-1 
      concentration and gene expression. There were significant direct relationships 
      between hepatic PON1 and MCP-1 concentrations (P = 0.005) and between PON1 and 
      the amount of activated stellate cells (P = 0.001). CONCLUSION: Our results from 
      this experimental model suggest a hepato-protective role for PON1 against 
      inflammation, fibrosis and liver disease mediated by MCP-1.
FAU - Marsillach, Judit
AU  - Marsillach J
AD  - Centre de Recerca Biomedica, Hospital Universitari de Sant Joan, Institut 
      d'Investigacions Sanitaries Pere Virgili, Universitat Rovira i Virgili, C, Sant 
      Joan s/n, 43201 Reus, Spain. jmarsillach@grupsagessa.cat
FAU - Camps, Jordi
AU  - Camps J
FAU - Ferre, Natalia
AU  - Ferre N
FAU - Beltran, Raul
AU  - Beltran R
FAU - Rull, Anna
AU  - Rull A
FAU - Mackness, Bharti
AU  - Mackness B
FAU - Mackness, Michael
AU  - Mackness M
FAU - Joven, Jorge
AU  - Joven J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090114
PL  - England
TA  - BMC Gastroenterol
JT  - BMC gastroenterology
JID - 100968547
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Free Radicals)
RN  - 0 (PPAR delta)
RN  - CL2T97X0V0 (Carbon Tetrachloride)
RN  - EC 3.1.8.1 (Aryldialkylphosphatase)
SB  - IM
MH  - Animals
MH  - Aryldialkylphosphatase/*physiology
MH  - Carbon Tetrachloride
MH  - Chemical and Drug Induced Liver Injury/etiology/*metabolism/*pathology
MH  - Chemokine CCL2/physiology
MH  - Free Radicals/metabolism
MH  - Liver Cirrhosis, Experimental/etiology/*metabolism/*pathology
MH  - Male
MH  - PPAR delta/*metabolism
MH  - Rats
MH  - Rats, Wistar
PMC - PMC2632645
EDAT- 2009/01/16 09:00
MHDA- 2009/05/06 09:00
PMCR- 2009/01/14
CRDT- 2009/01/16 09:00
PHST- 2008/08/28 00:00 [received]
PHST- 2009/01/14 00:00 [accepted]
PHST- 2009/01/16 09:00 [entrez]
PHST- 2009/01/16 09:00 [pubmed]
PHST- 2009/05/06 09:00 [medline]
PHST- 2009/01/14 00:00 [pmc-release]
AID - 1471-230X-9-3 [pii]
AID - 10.1186/1471-230X-9-3 [doi]
PST - epublish
SO  - BMC Gastroenterol. 2009 Jan 14;9:3. doi: 10.1186/1471-230X-9-3.