PMID- 19111613
OWN - NLM
STAT- MEDLINE
DCOM- 20090406
LR  - 20161126
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1792
IP  - 2
DP  - 2009 Feb
TI  - The role of redox status on chemokine expression in acute pancreatitis.
PG  - 148-54
LID - 10.1016/j.bbadis.2008.12.002 [doi]
AB  - This study focused on the involvement of oxidative stress in the mechanisms 
      mediating chemokine production in different cell sources during mild and severe 
      acute pancreatitis (AP) induced by bile-pancreatic duct obstruction (BPDO) and 
      3.5% NaTc, respectively. N-Acetylcysteine (NAC) was used as antioxidant 
      treatment. Pancreatic glutathione depletion, acinar overexpression of monocyte 
      chemoattractant protein-1 (MCP-1) and cytokine-induced neutrophil chemoattractant 
      (CINC), and activation of p38MAPK, NF-kappaB and STAT3 were found in both AP 
      models. NAC reduced the depletion of glutathione in BPDO- but not in NaTc-induced 
      AP, in which oxidative stress overwhelmed the antioxidant capability of NAC. As a 
      result, inhibition of the acinar chemokine expression and signalling pathways 
      occurs in mild, but not in severe AP. However, MCP-1 and CINC expressions in 
      whole pancreas and plasma chemokine levels were not reduced by NAC, even in 
      BPDO-induced AP, suggesting that in addition to acini, other pancreatic cells 
      produced chemokines by antioxidant resistant mechanisms. The high Il-6 plasma 
      levels found during AP, both in NAC-treated and non-treated rats, pointed out 
      cytokines as activating factors of chemokine expression in non-acinar cells. In 
      conclusion, from early AP oxidant-mediated MAPK, NF-kappaB and STAT3 activation 
      triggers the chemokine expression in acini but not in non-acinar cells.
FAU - Yubero, S
AU  - Yubero S
AD  - Department of Physiology and Pharmacology, University of Salamanca, 37007 
      Salamanca, Spain.
FAU - Ramudo, L
AU  - Ramudo L
FAU - Manso, M A
AU  - Manso MA
FAU - De Dios, I
AU  - De Dios I
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081209
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
RN  - 0 (Chemokines)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Chemokines/genetics/*metabolism
MH  - Gene Expression Regulation
MH  - Interleukin-6/blood
MH  - Male
MH  - NF-kappa B/metabolism
MH  - Oxidation-Reduction
MH  - Pancreatitis/genetics/*metabolism
MH  - Phosphorylation
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Wistar
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2008/12/30 09:00
MHDA- 2009/04/07 09:00
CRDT- 2008/12/30 09:00
PHST- 2008/09/12 00:00 [received]
PHST- 2008/11/12 00:00 [revised]
PHST- 2008/12/02 00:00 [accepted]
PHST- 2008/12/30 09:00 [entrez]
PHST- 2008/12/30 09:00 [pubmed]
PHST- 2009/04/07 09:00 [medline]
AID - S0925-4439(08)00250-0 [pii]
AID - 10.1016/j.bbadis.2008.12.002 [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 2009 Feb;1792(2):148-54. doi: 10.1016/j.bbadis.2008.12.002. 
      Epub 2008 Dec 9.