PMID- 27212619
OWN - NLM
STAT- MEDLINE
DCOM- 20170828
LR  - 20211204
IS  - 1590-3729 (Electronic)
IS  - 0939-4753 (Linking)
VI  - 26
IP  - 9
DP  - 2016 Sep
TI  - Sulforaphane reduces advanced glycation end products (AGEs)-induced inflammation 
      in endothelial cells and rat aorta.
PG  - 797-807
LID - S0939-4753(16)30026-6 [pii]
LID - 10.1016/j.numecd.2016.04.008 [doi]
AB  - BACKGROUND AND AIMS: Advanced glycation end products (AGEs)-receptor RAGE 
      interaction evokes oxidative stress and inflammatory reactions, thereby being 
      involved in endothelial cell (EC) damage in diabetes. Sulforaphane is generated 
      from glucoraphanin, a naturally occurring isothiocyanate found in widely consumed 
      cruciferous vegetables, by myrosinase. Sulforaphane has been reported to protect 
      against oxidative stress-mediated cell and tissue injury. However, effects of 
      sulforaphane on AGEs-induced vascular damage remain unclear. METHODS AND RESULTS: 
      In this study, we investigated whether and how sulforaphane could inhibit 
      inflammation in AGEs-exposed human umbilical vein ECs (HUVECs) and AGEs-injected 
      rat aorta. Sulforaphane treatment for 4 or 24 h dose-dependently inhibited the 
      AGEs-induced increase in RAGE, monocyte chemoattractant protein-1 (MCP-1), 
      intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion 
      molecular-1 (VCAM-1) gene expression in HUVECs. AGEs significantly stimulated 
      MCP-1 production by, and THP-1 cell adhesion to, HUVECs, both of which were 
      prevented by 1.6 muM sulforaphane. Sulforaphane significantly suppressed oxidative 
      stress generation and NADPH oxidase activation evoked by AGEs in HUVECs. 
      Furthermore, aortic RAGE, ICAM-1 and VCAM-1 expression in AGEs-injected rats were 
      increased, which were suppressed by simultaneous infusion of sulforaphane. 
      CONCLUSION: The present study demonstrated for the first time that sulforaphane 
      could inhibit inflammation in AGEs-exposed HUVECs and AGEs-infused rat aorta 
      partly by suppressing RAGE expression through its anti-oxidative properties. 
      Inhibition of the AGEs-RAGE axis by sulforaphane might be a novel therapeutic 
      target for vascular injury in diabetes.
CI  - Copyright (c) 2016 The Italian Society of Diabetology, the Italian Society for the 
      Study of Atherosclerosis, the Italian Society of Human Nutrition, and the 
      Department of Clinical Medicine and Surgery, Federico II University. Published by 
      Elsevier B.V. All rights reserved.
FAU - Matsui, T
AU  - Matsui T
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
FAU - Nakamura, N
AU  - Nakamura N
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
FAU - Ojima, A
AU  - Ojima A
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
FAU - Nishino, Y
AU  - Nishino Y
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
FAU - Yamagishi, S-I
AU  - Yamagishi SI
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan. Electronic 
      address: shoichi@med.kurume-u.ac.jp.
LA  - eng
PT  - Journal Article
DEP - 20160421
PL  - Netherlands
TA  - Nutr Metab Cardiovasc Dis
JT  - Nutrition, metabolism, and cardiovascular diseases : NMCD
JID - 9111474
RN  - 0 (AGER protein, human)
RN  - 0 (Ager protein, rat)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antioxidants)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Isothiocyanates)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor for Advanced Glycation End Products)
RN  - 0 (Sulfoxides)
RN  - GA49J4310U (sulforaphane)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Antioxidants/*pharmacology
MH  - Aorta/*drug effects/metabolism
MH  - Aortitis/chemically induced/metabolism/*prevention & control
MH  - Cell Adhesion Molecules/metabolism
MH  - Cell Line, Tumor
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - Endothelial Cells/*drug effects/metabolism
MH  - *Glycation End Products, Advanced
MH  - Human Umbilical Vein Endothelial Cells/drug effects/metabolism
MH  - Inflammation Mediators/metabolism
MH  - Isothiocyanates/*pharmacology
MH  - Male
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats, Wistar
MH  - Receptor for Advanced Glycation End Products/drug effects/genetics/metabolism
MH  - Sulfoxides
MH  - Time Factors
OTO - NOTNLM
OT  - AGEs
OT  - Atherosclerosis
OT  - Oxidative stress
OT  - RAGE
OT  - Sulforaphane
EDAT- 2016/05/24 06:00
MHDA- 2017/08/29 06:00
CRDT- 2016/05/24 06:00
PHST- 2016/01/14 00:00 [received]
PHST- 2016/04/04 00:00 [revised]
PHST- 2016/04/12 00:00 [accepted]
PHST- 2016/05/24 06:00 [entrez]
PHST- 2016/05/24 06:00 [pubmed]
PHST- 2017/08/29 06:00 [medline]
AID - S0939-4753(16)30026-6 [pii]
AID - 10.1016/j.numecd.2016.04.008 [doi]
PST - ppublish
SO  - Nutr Metab Cardiovasc Dis. 2016 Sep;26(9):797-807. doi: 
      10.1016/j.numecd.2016.04.008. Epub 2016 Apr 21.