PMID- 19241441
OWN - NLM
STAT- MEDLINE
DCOM- 20090714
LR  - 20211203
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 107
IP  - 1
DP  - 2009 May 1
TI  - Evodiamine and rutaecarpine inhibit migration by LIGHT via suppression of NADPH 
      oxidase activation.
PG  - 123-33
LID - 10.1002/jcb.22109 [doi]
AB  - LIGHT acted as a new player in the atherogenesis. The dried, unripe fruit of 
      Evodia Fructus (EF) has long been used as a traditional Chinese herbal medicine, 
      and is currently widely used for the treatment of headache, abdominal pain, 
      vomiting, colds and reduced blood circulation. Evodiamine and rutaecarpine are 
      active components of EF. In this study, we investigated the inhibitory effect of 
      evodiamine and rutaecarpine on LIGHT-induced migration in human monocytes. 
      Evodiamine and rutaecarpine decreased the LIGHT-induced production of ROS, IL-8, 
      monocyte chemoattractant protein-1 (MCP-1), TNF-alpha, and IL-6, as well as the 
      expression of chemokine receptor (CCR) 1, CCR2 and ICAM-1 and the phosphorylation 
      of the ERK 1/2 and p38 MAPK. Furthermore, NADPH oxidase assembly inhibitor, 
      AEBSF, blocked LIGHT-induced migration and activation of CCR1, CCR2, ICAM-1, and 
      MAPK such as ERK and p38 in a manner similar to evodiamine and rutaecarpine. 
      These findings indicate that the inhibitory effects of evodiamine and 
      rutaecarpine on LIGHT-induced migration and the activation of CCR1, CCR2, ICAM-1, 
      ERK, and p38 MAPK occurs via decreased ROS production and NADPH oxidase 
      activation. Taken together, these results indicate that evodiamine and 
      rutaecarpine have the potential for use as an anti-atherosclerosis agent.
FAU - Heo, Sook-Kyoung
AU  - Heo SK
AD  - Department of Prescriptionology, Cardiovascular Medical Research Center, 
      University of Dongguk, Gyeongju City, Gyeongbuk, Republic of Korea. 
      hsk927@yahoo.com
FAU - Yun, Hyun-Jeong
AU  - Yun HJ
FAU - Yi, Hyo-Seung
AU  - Yi HS
FAU - Noh, Eui-Kyu
AU  - Noh EK
FAU - Park, Sun-Dong
AU  - Park SD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (CCR2 protein, human)
RN  - 0 (Indole Alkaloids)
RN  - 0 (Phosphoproteins)
RN  - 0 (Plant Extracts)
RN  - 0 (Quinazolines)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptors, CCR2)
RN  - 0 (TNFSF14 protein, human)
RN  - 0 (Tumor Necrosis Factor Ligand Superfamily Member 14)
RN  - 0 (neutrophil cytosol factor 40K)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 8XZV289PRY (rutecarpine)
RN  - C01825BVNL (evodiamine)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 2.7.1.- (SNF1-related protein kinases)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Cell Line
MH  - Cell Movement/drug effects
MH  - Enzyme Activation/drug effects
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Extracellular Signal-Regulated MAP Kinases/drug effects/metabolism
MH  - Flow Cytometry
MH  - Humans
MH  - Immunoblotting
MH  - Indole Alkaloids/*pharmacology
MH  - Intercellular Adhesion Molecule-1/drug effects/metabolism
MH  - Monocytes/*drug effects/metabolism
MH  - NADPH Oxidases/*drug effects/metabolism
MH  - Phosphoproteins/drug effects/metabolism
MH  - Phosphorylation/drug effects
MH  - Plant Extracts/*pharmacology
MH  - Protein Serine-Threonine Kinases/drug effects/metabolism
MH  - Quinazolines/*pharmacology
MH  - Reactive Oxygen Species/metabolism
MH  - Receptors, CCR2/drug effects/metabolism
MH  - Tumor Necrosis Factor Ligand Superfamily Member 14/*metabolism
MH  - p38 Mitogen-Activated Protein Kinases/drug effects/metabolism
EDAT- 2009/02/26 09:00
MHDA- 2009/07/15 09:00
CRDT- 2009/02/26 09:00
PHST- 2009/02/26 09:00 [entrez]
PHST- 2009/02/26 09:00 [pubmed]
PHST- 2009/07/15 09:00 [medline]
AID - 10.1002/jcb.22109 [doi]
PST - ppublish
SO  - J Cell Biochem. 2009 May 1;107(1):123-33. doi: 10.1002/jcb.22109.