PMID- 19652376
OWN - NLM
STAT- MEDLINE
DCOM- 20100222
LR  - 20220311
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 32
IP  - 8
DP  - 2009 Aug
TI  - Effect of caffeic acid on tumor necrosis factor-alpha-induced vascular 
      inflammation in human umbilical vein endothelial cells.
PG  - 1371-7
AB  - Recruitment of specific leukocyte subpopulations at the site of inflammation 
      requires a series of cell adhesion molecules (CAMs)-mediated interactions. The 
      major CAMs, viz., intracellular adhesion molecule-1 (ICAM-1), vascular cell 
      adhesion molecule-1 (VCAM-1), and E-selectin are expressed on endothelium in 
      response to various cytokines. Caffeic acid (CA), a natural phenolic compound 
      from herbs and other sources, has been shown to prevent cardiovascular diseases. 
      We investigated the effect of CA on the expression of CAMs by human umbilical 
      vein endothelial cells (HUVECs) stimulated with tumor necrosis factor 
      (TNF-alpha). Adhesion of monocytes to CA-treated HUVECs was evaluated by 
      co-culture experiments using 2,7-bis(2-carboxyethyl)-5(6)-carboxyfluorescein 
      acetoxymethylester (BCECF-AM) labeling of U937 cells. The expression of adhesion 
      and chemoattractant molecules was evaluated by Western blot and reverse 
      transcription-polymerase chain reaction (RT-PCR), respectively. CA significantly 
      inhibited the TNF-alpha-induced increase in U937 monocyte adhesion to HUVECs as 
      well as decreased the protein and mRNA expression levels of CAMs on HUVECs. CA 
      also inhibited the mRNA expression of monocyte chemoattractant protein-1 (MCP-1) 
      and interleukin-8 (IL-8). The involvement of nuclear factor (NF)-kappaB in the 
      transcriptional control of CAMs protein was assessed by degradation of inhibitory 
      (I)kappaB and nuclear translocation of NF-kappaB using Western blotting and 
      immunofluorescence staining. CA attenuated TNF-alpha-induced IkappaB degradation 
      and NF-kappaB translocation from cytosol to the nucleus. In conclusion, 
      TNF-alpha-induced NF-kappaB-DNA complex formation was inhibited by CA. CA reduced 
      TNF-alpha-induced endothelial adhesiveness to HUVECs by inhibiting transcription 
      factor activation, and CAMs expression suggesting its potential role in 
      atherosclerosis diseases.
FAU - Moon, Mi Kyoung
AU  - Moon MK
AD  - Professional Graduate School of Oriental Medicine, Wonkwang University, Iksan, 
      Jeonbuk, Republic of Korea.
FAU - Lee, Yun Jung
AU  - Lee YJ
FAU - Kim, Jin Sook
AU  - Kim JS
FAU - Kang, Dae Gill
AU  - Kang DG
FAU - Lee, Ho Sub
AU  - Lee HS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Caffeic Acids)
RN  - 0 (Chemokine CCL2)
RN  - 0 (E-Selectin)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - U2S3A33KVM (caffeic acid)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology
MH  - Blotting, Western
MH  - Caffeic Acids/*pharmacology
MH  - Cell Adhesion/drug effects/immunology
MH  - Cell Culture Techniques
MH  - Chemokine CCL2/biosynthesis
MH  - Coculture Techniques
MH  - E-Selectin/biosynthesis
MH  - Endothelial Cells/cytology/*drug effects/immunology/metabolism
MH  - Endothelium, Vascular/cytology/*drug effects/immunology/metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Inflammation
MH  - Monocytes/cytology/*drug effects/immunology/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Transcription Factor RelA/metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology/*physiology
MH  - U937 Cells
MH  - Vascular Cell Adhesion Molecule-1/biosynthesis
EDAT- 2009/08/05 09:00
MHDA- 2010/02/23 06:00
CRDT- 2009/08/05 09:00
PHST- 2009/08/05 09:00 [entrez]
PHST- 2009/08/05 09:00 [pubmed]
PHST- 2010/02/23 06:00 [medline]
AID - JST.JSTAGE/bpb/32.1371 [pii]
AID - 10.1248/bpb.32.1371 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2009 Aug;32(8):1371-7. doi: 10.1248/bpb.32.1371.