PMID- 22965302
OWN - NLM
STAT- MEDLINE
DCOM- 20140226
LR  - 20211021
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 6
IP  - 6
DP  - 2012 Dec
TI  - Naringin inhibits chemokine production in an LPS-induced RAW 264.7 macrophage 
      cell line.
PG  - 1343-50
LID - 10.3892/mmr.2012.1072 [doi]
AB  - Naringin has been reported to act as an effective anti-inflammatory compound. In 
      a previous study, we demonstrated that the anti-inflammatory effect of naringin 
      on lipopolysaccharide (LPS)-induced acute lung injury in mice correlated with the 
      inhibition of the nuclear factor-kappaB (NF-kappaB) pathway. However, the effects and 
      mechanism of action of naringin on LPS-induced chemokine expression are not yet 
      fully understood. This study aimed to evaluate the effect of naringin on 
      chemokine expression in LPS-induced RAW 264.7 macrophages and to provide insights 
      into the possible underlying mechanisms. We found that the in vitro pre-treatment 
      with naringin led to a significant attenuation in the LPS-induced secretion of 
      interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and macrophage 
      inflammatory protein-1alpha (MIP-1alpha). RT-qPCR demonstrated that naringin 
      significantly reduced the LPS-induced upregulation of IL-8, MCP-1 and MIP-1alpha mRNA 
      expression in a dose-dependent manner. Additionally, western blot analysis 
      revealed that naringin effectively suppressed NF-kappaB activation by inhibiting the 
      degradation of IkappaB-alpha and the translocation of p65. Naringin also attenuated MAPK 
      activation by inhibiting the phosphorylation of ERK1/2, JNK and p38 MAPK. Taken 
      together, these demonstrate that naringin reduces IL-8, MCP-1 and MIP-1alpha 
      secretion and mRNA expression, possibly by blocking the activation of the NF-kappaB 
      and MAPK signaling pathways in LPS-induced RAW 264.7 macrophages.
FAU - Liu, Ying
AU  - Liu Y
AD  - Key Laboratory of Gene Engineering of the Ministry of Education and Guangdong Key 
      Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, 
      Guangzhou, Guangdong 510275, P.R. China.
FAU - Su, Wei-wei
AU  - Su WW
FAU - Wang, Sheng
AU  - Wang S
FAU - Li, Pei-bo
AU  - Li PB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120910
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokines)
RN  - 0 (Flavanones)
RN  - 0 (I-kappa B Proteins)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Nfkbia protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Transcription Factor RelA)
RN  - 139874-52-5 (NF-KappaB Inhibitor alpha)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - N7TD9J649B (naringin)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Chemokine CCL3/genetics/metabolism
MH  - Chemokines/genetics/*metabolism
MH  - Flavanones/*pharmacology
MH  - Gene Expression/*drug effects
MH  - I-kappa B Proteins/metabolism
MH  - Interleukin-8/genetics/metabolism
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - Lipopolysaccharides/toxicity
MH  - Macrophages/drug effects
MH  - Mice
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinase 3/metabolism
MH  - NF-KappaB Inhibitor alpha
MH  - NF-kappa B/metabolism
MH  - Phosphorylation/drug effects
MH  - RNA, Messenger/metabolism
MH  - Receptors, CCR2/genetics/metabolism
MH  - Signal Transduction/drug effects
MH  - Transcription Factor RelA/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
OTO - NOTNLM
OT  - naringin
OT  - lipopolysaccharide
OT  - interleukin-8
OT  - monocyte chemoattractant protein-1
OT  - macrophage inflammatory protein-1alpha
OT  - nuclear factor-kappaB
OT  - mitogen-activated protein kinase
EDAT- 2012/09/12 06:00
MHDA- 2014/02/27 06:00
CRDT- 2012/09/12 06:00
PHST- 2012/04/28 00:00 [received]
PHST- 2012/08/28 00:00 [accepted]
PHST- 2012/09/12 06:00 [entrez]
PHST- 2012/09/12 06:00 [pubmed]
PHST- 2014/02/27 06:00 [medline]
AID - 10.3892/mmr.2012.1072 [doi]
PST - ppublish
SO  - Mol Med Rep. 2012 Dec;6(6):1343-50. doi: 10.3892/mmr.2012.1072. Epub 2012 Sep 10.