Document Detail


CML-1 inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in endothelial cells through inhibition of IkBalpha kinase.
MedLine Citation:
PMID:  16920299     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
CML-1 is a purified extract from a mixture of 13 oriental herbs (Achyranthis Radix, Angelicae Gigantis Radix, Cinnamomi Cortex Spissus, Eucommiae Cortex, Glycyrrhizae Radix, Hoelen, Lycii Fructus, Paeoniae Radix, Rehmanniae Radix Preparata and Atractylodis Rhizoma, Zingiberis Rhizoma, Zizyphi Semen, Acori Graminei Rhizoma) that have been widely used for the treatment of inflammatory diseases in Asia. Since our previous study has been shown to have the anti-inflammatory activity of CML-1 in vivo and the upregulation of adhesion molecules in response to numerous inducing factors is associated with inflammation, this study examined the effect of CML-1 on the expression of adhesion molecules induced by TNF-alpha in cultured human umbilical vein endothelial cells (HUVECs). Preincubation of HUVECs for 20h with CML-1 (1-100mug/ml) dose-dependently inhibited TNF-alpha (10ng/ml)-induced adhesion of THP-1 monocytic cells, as well as mRNA and protein expression of E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). CML-1 was also shown to inhibit NK-kB activation induced by TNF-alpha. Furthermore, CML-1 inhibited TNF-alpha-induced IkB kinase activation, subsequent degradation of IkBalpha, and nuclear translocation of NK-kB. Evidence presented in this report demonstrated that CML-1 inhibited the adhesive capacity of HUVEC and the TNF-alpha-mediated induction of E-selectin, ICAM-1 and VCAM-1 in HUVEC by inhibiting the IkB/NF-kB signaling pathway at the level of IkB kinase, which may explain the ability of CML-1 to suppress inflammation and modulate the immune response.
Authors:
Seong-Ji Mo; Eun-Wha Son; Sung-Ryul Lee; Sun-Mee Lee; Dae-Hee Shin; Suhkneung Pyo
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Publication Detail:
Type:  Journal Article     Date:  2006-07-11
Journal Detail:
Title:  Journal of ethnopharmacology     Volume:  109     ISSN:  0378-8741     ISO Abbreviation:  J Ethnopharmacol     Publication Date:  2007 Jan 
Date Detail:
Created Date:  2006-12-04     Completed Date:  2007-04-12     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7903310     Medline TA:  J Ethnopharmacol     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  78-86     Citation Subset:  IM    
Affiliation:
College of Pharmacy, Sungkyunkwan University, Suwon City, Kyunggi-do 440-746, Republic of Korea.
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MeSH Terms
Descriptor/Qualifier:
Biotransformation / drug effects
Blotting, Western
Cell Adhesion / drug effects
Cell Adhesion Molecules / biosynthesis*
Cells, Cultured
Chromatography, High Pressure Liquid
E-Selectin / biosynthesis
Electrophoretic Mobility Shift Assay
Endothelial Cells / drug effects,  metabolism*
Enzyme Inhibitors / pharmacology*
Enzyme-Linked Immunosorbent Assay
Humans
I-kappa B Kinase / antagonists & inhibitors*
Immunoprecipitation
Intercellular Adhesion Molecule-1 / biosynthesis
NF-kappa B / drug effects*
Plant Extracts / pharmacology*
Reverse Transcriptase Polymerase Chain Reaction
Tumor Necrosis Factor-alpha / antagonists & inhibitors*,  pharmacology
Vascular Cell Adhesion Molecule-1 / biosynthesis
Chemical
Reg. No./Substance:
0/CML-1 plant extract; 0/Cell Adhesion Molecules; 0/E-Selectin; 0/Enzyme Inhibitors; 0/NF-kappa B; 0/Plant Extracts; 0/Tumor Necrosis Factor-alpha; 0/Vascular Cell Adhesion Molecule-1; 126547-89-5/Intercellular Adhesion Molecule-1; EC 2.7.11.10/I-kappa B Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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