PMID- 23291378
OWN - NLM
STAT- MEDLINE
DCOM- 20130618
LR  - 20181202
IS  - 1873-5487 (Electronic)
IS  - 0188-4409 (Linking)
VI  - 44
IP  - 1
DP  - 2013 Jan
TI  - Genistein inhibits ox-LDL-induced VCAM-1, ICAM-1 and MCP-1 expression of HUVECs 
      through heme oxygenase-1.
PG  - 13-20
LID - S0188-4409(12)00340-2 [pii]
LID - 10.1016/j.arcmed.2012.12.001 [doi]
AB  - BACKGROUND AND AIMS: Genistein, a principal component of soybean isoflavones, 
      plays an important role in the prevention of atherosclerosis. However, the 
      detailed mechanisms have not been fully investigated. The aims of this study were 
      to evaluate the anti-atherosclerotic effect and investigate potential 
      pharmacological mechanism of genistein. METHODS: A model of oxidized low-density 
      lipoprotein (ox-LDL)-induced injury in on human umbilical vein endothelial cells 
      (HUVECs) was established to evaluate the protective role of genistein. 
      Macrophage/monocyte chemoattractant protein-1 (MCP-1), vascular cellular adhesion 
      molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) secretion and 
      their messenger RNA transcription were observed via enzyme-linked immunosorbent 
      assay (ELISA) and reverse transcriptase PCR (RT-PCR). Meanwhile, the study 
      investigated the role of Nrf2/HO-1 pathway during the process. RESULTS: 
      Pretreatment with genistein markedly reduced ox-LDL-induced MCP-1, VCAM-1 and 
      ICAM-1 secretion and mRNA transcription, which was further decreased by the 
      inducer of HO and reversed by the inhibitor of HO; additionally, the effects were 
      accompanied with upregulating HO-1 mRNA and protein expression and markedly 
      abolished with Nrf2 siRNA. CONCLUSIONS: Anti-inflammatory effect of genistein on 
      endothelial cells may be associated with the activation of Nrf2/HO-1 pathway.
CI  - Copyright (c) 2013 IMSS. Published by Elsevier Inc. All rights reserved.
FAU - Zhang, Hua-ping
AU  - Zhang HP
AD  - Key Laboratory of Ministry of Education, Shanxi Medical University, Taiyuan, PR 
      China. hpzhang7302@yahoo.com.cn
FAU - Zheng, Feng-li
AU  - Zheng FL
FAU - Zhao, Jia-hui
AU  - Zhao JH
FAU - Guo, Dong-xing
AU  - Guo DX
FAU - Chen, Xiao-long
AU  - Chen XL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130103
PL  - United States
TA  - Arch Med Res
JT  - Archives of medical research
JID - 9312706
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (ICAM1 protein, human)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NFE2L2 protein, human)
RN  - 0 (RNA, Messenger)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 0 (oxidized low density lipoprotein)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - DH2M523P0H (Genistein)
RN  - EC 1.14.14.18 (HMOX1 protein, human)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
SB  - IM
MH  - Cell Nucleus/drug effects/metabolism
MH  - Cell Survival/drug effects
MH  - Chemokine CCL2/biosynthesis/genetics/*metabolism
MH  - Down-Regulation/drug effects
MH  - Genistein/*pharmacology
MH  - Heme Oxygenase-1/genetics/*metabolism
MH  - Human Umbilical Vein Endothelial Cells/cytology/*drug 
      effects/enzymology/metabolism
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/*biosynthesis/genetics/metabolism
MH  - Lipoproteins, LDL/*pharmacology
MH  - NF-E2-Related Factor 2/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Vascular Cell Adhesion Molecule-1/*biosynthesis/genetics/metabolism
EDAT- 2013/01/08 06:00
MHDA- 2013/06/19 06:00
CRDT- 2013/01/08 06:00
PHST- 2012/07/27 00:00 [received]
PHST- 2012/11/26 00:00 [accepted]
PHST- 2013/01/08 06:00 [entrez]
PHST- 2013/01/08 06:00 [pubmed]
PHST- 2013/06/19 06:00 [medline]
AID - S0188-4409(12)00340-2 [pii]
AID - 10.1016/j.arcmed.2012.12.001 [doi]
PST - ppublish
SO  - Arch Med Res. 2013 Jan;44(1):13-20. doi: 10.1016/j.arcmed.2012.12.001. Epub 2013 
      Jan 3.