PMID- 28448865
OWN - NLM
STAT- MEDLINE
DCOM- 20180326
LR  - 20180326
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 91
DP  - 2017 Jul
TI  - Glycolipids from spinach suppress LPS-induced vascular inflammation through eNOS 
      and NK-kappaB signaling.
PG  - 111-120
LID - S0753-3322(17)30153-1 [pii]
LID - 10.1016/j.biopha.2017.04.052 [doi]
AB  - Glycolipids are the major constituent of the thylakoid membrane of higher plants 
      and have a variety of biological and pharmacological activities. However, 
      anti-inflammatory effects of glycolipids on vascular endothelial cells have not 
      been elucidated. Here, we investigated the effect of glycolipids extracted from 
      spinach on lipopolysaccharides (LPS)-induced endothelial inflammation and 
      evaluated the underlying molecular mechanisms. Treatment with glycolipids from 
      spinach had no cytotoxic effects on cultured human umbilical vein endothelial 
      cells (HUVECs) and significantly blocked the expression of LPS-induced 
      interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1), vascular cell 
      adhesion molecule-1 (VCAM-1), and intracellular adhesion molecule-1 (ICAM-1) in 
      them. Glycolipids treatment also effectively suppressed monocyte adhesion to 
      HUVECs. Treatment with glycolipids inhibited LPS-induced NF-kappaB phosphorylation 
      and nuclear translocation. In addition, glycolipids treatment significantly 
      promoted endothelial nitric oxide synthase (eNOS) activation and nitric oxide 
      (NO) production in HUVECs. Furthermore, glycolipids treatment blocked LPS-induced 
      inducible NOS (iNOS) expression in HUVECs. Pretreatment with a NOS inhibitor 
      attenuated glycolipids-induced suppression of NF-kappaB activation and adhesion 
      molecule expression, and abolished the glycolipids-mediated suppression of 
      monocyte adhesion to HUVECs. These results indicate that glycolipids suppress 
      LPS-induced vascular inflammation through attenuation of the NF-kappaB pathway by 
      increasing NO production in endothelial cells. These findings suggest that 
      glycolipids from spinach may have a potential therapeutic use for inflammatory 
      vascular diseases.
CI  - Copyright (c) 2017 Elsevier Masson SAS. All rights reserved.
FAU - Ishii, Masakazu
AU  - Ishii M
AD  - Department of Oral and Maxillofacial Prosthodontics, Kagoshima University 
      Graduate school of Medical and Dental Science, Kagoshima 890-8544, Japan. 
      Electronic address: masai@dent.kagoshima-u.ac.jp.
FAU - Nakahara, Tatsuo
AU  - Nakahara T
AD  - Maruzen Pharmaceuticals Co., Ltd., Hiroshima 729-3102, Japan.
FAU - Araho, Daisuke
AU  - Araho D
AD  - Maruzen Pharmaceuticals Co., Ltd., Hiroshima 729-3102, Japan.
FAU - Murakami, Juri
AU  - Murakami J
AD  - Department of Oral and Maxillofacial Prosthodontics, Kagoshima University 
      Graduate school of Medical and Dental Science, Kagoshima 890-8544, Japan; 
      Department of Oral and Maxillofacial Surgery, Kagoshima University Graduate 
      School of Medical and Dental Science, Kagoshima 890-8544, Japan.
FAU - Nishimura, Masahiro
AU  - Nishimura M
AD  - Department of Oral and Maxillofacial Prosthodontics, Kagoshima University 
      Graduate school of Medical and Dental Science, Kagoshima 890-8544, Japan.
LA  - eng
PT  - Journal Article
DEP - 20170424
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Cytokines)
RN  - 0 (Glycolipids)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
SB  - IM
MH  - Blood Vessels/*pathology
MH  - Cell Adhesion/drug effects
MH  - Cell Survival/drug effects
MH  - Cytokines/metabolism
MH  - Glycolipids/isolation & purification/pharmacology/*therapeutic use
MH  - Human Umbilical Vein Endothelial Cells/drug effects/metabolism/pathology
MH  - Humans
MH  - Inflammation/*drug therapy/*enzymology/pathology
MH  - Inflammation Mediators/metabolism
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Lipopolysaccharides
MH  - Monocytes/cytology
MH  - NF-kappa B/*metabolism
MH  - Nitric Oxide Synthase Type III/*metabolism
MH  - *Signal Transduction
MH  - Spinacia oleracea/*chemistry
MH  - Vascular Cell Adhesion Molecule-1/metabolism
OTO - NOTNLM
OT  - Anti-inflammation
OT  - Endothelial cells
OT  - Glycolipids
OT  - NF-kappaB
OT  - eNOS
EDAT- 2017/04/28 06:00
MHDA- 2018/03/27 06:00
CRDT- 2017/04/28 06:00
PHST- 2017/01/11 00:00 [received]
PHST- 2017/04/07 00:00 [revised]
PHST- 2017/04/13 00:00 [accepted]
PHST- 2017/04/28 06:00 [pubmed]
PHST- 2018/03/27 06:00 [medline]
PHST- 2017/04/28 06:00 [entrez]
AID - S0753-3322(17)30153-1 [pii]
AID - 10.1016/j.biopha.2017.04.052 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2017 Jul;91:111-120. doi: 10.1016/j.biopha.2017.04.052. Epub 
      2017 Apr 24.