Essential oil from Fructus Alpinia zerumbet (fruit of Alpinia zerumbet (Pers.) Burtt.et Smith) protected against aortic endothelial cell injury and inflammation in vitro and in vivo.
Alpinia
Animals
Anti-Inflammatory Agents
/ pharmacology
Aorta
/ cytology
Cells, Cultured
Endothelial Cells
/ drug effects
Fruit
Humans
Intercellular Adhesion Molecule-1
/ genetics
Lipopolysaccharides
Male
Mice
NF-kappa B
/ metabolism
Oils, Volatile
/ pharmacology
Toll-Like Receptor 4
/ genetics
Vascular Cell Adhesion Molecule-1
/ genetics
Endothelial injury
Fructus Alpinia zerumbet
Inflammation
LPS
NF-κB
TLR4
Journal
Journal of ethnopharmacology
ISSN: 1872-7573
Titre abrégé: J Ethnopharmacol
Pays: Ireland
ID NLM: 7903310
Informations de publication
Date de publication:
12 Jun 2019
12 Jun 2019
Historique:
received:
18
09
2018
revised:
05
03
2019
accepted:
05
03
2019
pubmed:
19
3
2019
medline:
20
8
2019
entrez:
19
3
2019
Statut:
ppublish
Résumé
Fructus Alpinia zerumbet (FAZ), a dry and ripe fruit of Alpinia zerumbet (Pers.) Burtt. et Smith, is widely used as a spice to treat cardiovascular diseases in clinic as a miao folk medicine in Guizhou Province of China. Essential oil extracted from FAZ (EOFAZ) is the key bioactive ingredients. This study aimed to examine the effects and mechanisms of EOFAZ on lipopolysaccharide (LPS)-induced endothelial cell injury, inflammation and apoptosis in vitro and in vivo. For the in vitro study, LPS-treated human aortic endothelial cells were used to perform PCR, western blot analysis and immunofluorescence. For the in vivo study, male mouse were divided into four groups, vehicle control group and LPS group received 0.5% Tween-80 in saline; and two EOFAZ groups receive different dose of EOFAZ (90 mg kg We found that EOFAZ completely prevented LPS-induced HAEC activation and inflammation in vitro and in vivo, as assessed by expression of endothelial adhesion molecules, ICAM-1 and VCAM-1. Similarly, EOFAZ significantly blunted LPS-induced endothelial injury, as tested by MTT assay, LDH release and caspase-3 activation. We further demonstrated that TLR4-dependent NF-κB signaling may be involved in the process. EOFAZ protected against LPS-induced endothelial cell injury and inflammation likely via inhibition of TLR4-dependent NF-κB signaling.
Identifiants
pubmed: 30880260
pii: S0378-8741(18)33244-6
doi: 10.1016/j.jep.2019.03.011
pii:
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Lipopolysaccharides
0
NF-kappa B
0
Oils, Volatile
0
Toll-Like Receptor 4
0
Vascular Cell Adhesion Molecule-1
0
Intercellular Adhesion Molecule-1
126547-89-5
Types de publication
Journal Article
Langues
eng
Pagination
149-158Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.