Etlingera pavieana extract attenuates TNF-α induced vascular adhesion molecule expression in human endothelial cells through NF-κB and Akt/JNK pathways

被引:0
作者
Klaokwan Srisook
Kamonporn Potiprasart
Songklod Sarapusit
Chang-Shin Park
Ekaruth Srisook
机构
[1] Faculty of Science,Department of Biochemistry and Research Unit of Natural Bioactive Compounds for Healthcare Products Development
[2] Burapha University,Center of Excellence for Innovation in Chemistry, Faculty of Science
[3] Burapha University,Department of Pharmacology, Hypoxia
[4] College of Medicine,Related Disease Research Center
[5] Inha Research Institute for Medical Sciences,Department of Chemistry and Research Unit of Natural Bioactive Compounds for Healthcare Products Development, Faculty of Science
[6] Inha University,undefined
[7] Burapha University,undefined
来源
Inflammopharmacology | 2020年 / 28卷
关键词
Inflammation; Cell adhesion molecules; Endothelial cell;
D O I
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中图分类号
学科分类号
摘要
The aim of this study was to determine whether ethanol extracts of Etlingera pavieana rhizomes (EPE) can inhibit the expression of ICAM-1 and VCAM-1 in TNF-α-stimulated human vascular endothelial cells. EPE significantly reduced ICAM-1 and VCAM-1 expression in a concentration-dependent manner. EPE also suppressed phospho-IκB level and nuclear translocation of NF-κB. EPE significantly inhibited phosphorylation of JNK and c-Jun, a major component of AP-1, but had no effects on ERK and p38 MAPK pathways. Akt phosphorylation was increased in the presence of EPE, and wortmannin and SP600125 reversed the inhibitory effects of EPE on ICAM-1 and VCAM-1 expression. Furthermore, the active EPE constituents 4-methoxycinnamyl p-coumarate and trans-4-methoxycinnamaldehyde attenuated TNF-α-induced expression of ICAM-1 and VCAM-1. Taken together, our data indicate that EPE protects against vascular inflammation in endothelial cells, in part via NF-κB and Akt/JNK signalings. In future studies, E. pavieana may be developed as a therapeutic agent or dietary supplement for treating and preventing inflammatory diseases.
引用
收藏
页码:1649 / 1662
页数:13
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