PMID- 22673210
OWN - NLM
STAT- MEDLINE
DCOM- 20121030
LR  - 20161125
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 52
IP  - 3-4
DP  - 2012 Oct
TI  - Inhibition of the transcription factor c-Jun by the MAPK family, and not the 
      NF-kappaB pathway, suggests that peanut extract has anti-inflammatory properties.
PG  - 125-32
LID - 10.1016/j.molimm.2012.05.007 [doi]
AB  - BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is involved in inflammatory responses 
      in atherosclerosis. We propose an in vitro cellular assay to evaluate the 
      anti-inflammatory mechanisms of potential modifiers such as food extracts. In the 
      current model we assessed an anti-inflammatory effect of polyphenol-rich peanut 
      extract in lipopolysaccharide (LPS)-induced THP-1 monocytes. METHODS: THP-1 
      monocytes were incubated with peanut extract (5, 25, 50 and 100 mug/mL) consisting 
      of 39% flavonols, 37% flavanols and 24% phenolic acid (or BAY 11-7082 (5 muM) as 
      experiment control) for 1 h and then stimulated with LPS (500 ng/mL) for 4 h. 
      Cytotoxicity was measured as lactate dehydrogenase (LDH) activity release. NF-kappaB 
      and MAPK family were determined by TransAm kit while TNF-alpha mRNA levels and its 
      mRNA stability by RT-PCR. Intra- and extracellular TNF-alpha protein was measured by 
      ELISA, and TNF-alpha converting enzyme (TACE) activity by a fluorimetric assay. 
      RESULTS: Peanut extract inhibited the maximal LPS-induced extracellular TNF-alpha 
      protein secretion by 18%, 29% and 47% at 25, 50 and 100 mug/mL, respectively 
      (P<0.05). LPS stimulation revealed that 85% of TNF-alpha was released extracellularly 
      while 15% remained intracellular. Peanut extract did not modify NF-kappaB but, 
      instead, reduced c-Jun transcription factor activity (P<0.05), decreased TNF-alpha 
      mRNA (albeit non-significantly) and had no effect on mRNA stability and TACE 
      activity. CONCLUSION: Polyphenol-rich peanut extract reduces extracellular TNF-alpha 
      protein by inhibiting c-Jun transcription factor from MAPK family, suggesting an 
      anti-inflammatory effect. The proposed THP-1 monocyte model could be used to 
      assess food extract impact (site and size effects) on the inflammation pathway.
CI  - Copyright (c) 2012 Elsevier Ltd. All rights reserved.
FAU - Catalan, Ursula
AU  - Catalan U
AD  - Unitat de Recerca en Lipids i Arteriosclerosi, CIBERDEM, Hospital Universitari 
      Sant Joan, IISPV, Universitat Rovira i Virgili, Reus, Tarragona, Spain.
FAU - Fernandez-Castillejo, Sara
AU  - Fernandez-Castillejo S
FAU - Angles, Neus
AU  - Angles N
FAU - Morello, Jose Ramon
AU  - Morello JR
FAU - Yebras, Marti
AU  - Yebras M
FAU - Sola, Rosa
AU  - Sola R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120604
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Plant Extracts)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.86 (ADAM17 Protein)
RN  - EC 3.4.24.86 (ADAM17 protein, human)
SB  - IM
MH  - ADAM Proteins/metabolism
MH  - ADAM17 Protein
MH  - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology
MH  - *Arachis
MH  - Cell Line
MH  - Cell Line, Tumor
MH  - Humans
MH  - JNK Mitogen-Activated Protein Kinases/*antagonists & inhibitors
MH  - L-Lactate Dehydrogenase/metabolism
MH  - Lipopolysaccharides/immunology
MH  - Monocytes/drug effects/*immunology/metabolism
MH  - NF-kappa B/*metabolism
MH  - Plant Extracts/*pharmacology
MH  - Signal Transduction/drug effects
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2012/06/08 06:00
MHDA- 2012/10/31 06:00
CRDT- 2012/06/08 06:00
PHST- 2011/12/22 00:00 [received]
PHST- 2012/05/08 00:00 [revised]
PHST- 2012/05/09 00:00 [accepted]
PHST- 2012/06/08 06:00 [entrez]
PHST- 2012/06/08 06:00 [pubmed]
PHST- 2012/10/31 06:00 [medline]
AID - S0161-5890(12)00280-5 [pii]
AID - 10.1016/j.molimm.2012.05.007 [doi]
PST - ppublish
SO  - Mol Immunol. 2012 Oct;52(3-4):125-32. doi: 10.1016/j.molimm.2012.05.007. Epub 
      2012 Jun 4.