PMID- 24852948
OWN - NLM
STAT- MEDLINE
DCOM- 20150414
LR  - 20190212
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 33
IP  - 5
DP  - 2014
TI  - Green tea polyphenol epigallocatechin-3-gallate inhibits TNF-alpha-induced production 
      of monocyte chemoattractant protein-1 in human umbilical vein endothelial cells.
PG  - 1349-58
LID - 10.1159/000358702 [doi]
AB  - AIMS: Epigallocatechin-3-gallate (EGCG), a major catechin found in green tea, 
      displays a variety of pharmacological properties and recently received attention 
      as a prospective dietary intervention in cardiovascular diseases (CVD). This 
      study was conducted to test the hypothesis that EGCG was able to inhibit tumor 
      necrosis factor-alpha (TNF-alpha)-induced production of monocyte chemoattractant 
      protein-1 (MCP-1) in human umbilical vein endothelial cells (HUVECs) and 
      investigated the underlying molecular mechanisms. METHODS: The inhibitory effect 
      of EGCG on TNF-alpha-induced expression of MCP-1 was measured using ELISA and 
      RT-qPCR. The effect of EGCG on TNF-alpha-induced nuclear factor-kappa B (NF-kappaB) 
      activation was investigated by western blot and luciferase assays. Monocyte 
      adhesion assay was detected by microscope. RESULTS: EGCG significantly suppressed 
      the TNF-alpha-induced protein and mRNA expression of MCP-1. Investigation of the 
      mechanism suggested that EGCG suppressed the TNF-alpha-mediated NF-kappaB activation. In 
      addition, the 67-kD laminin receptor (67LR) was involved in EGCG-mediated 
      suppression of MCP-1 generation. Furthermore, EGCG potently inhibited monocyte 
      adhesion to activated HUVECs. CONCLUSION: EGCG suppresses TNF-alpha-induced MCP-1 
      expression in HUVECs. This effect was mediated by 67LR and was via the inhibition 
      of NF-kappaB activation. Our results demonstrated that EGCG might be a possible 
      medicine for CVD prevention and treatment.
CI  - (c) 2014 S. Karger AG, Basel.
FAU - Wang, Ze-Mu
AU  - Wang ZM
AD  - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, China.
FAU - Gao, Wei
AU  - Gao W
FAU - Wang, Hao
AU  - Wang H
FAU - Zhao, Di
AU  - Zhao D
FAU - Nie, Zhen-Lin
AU  - Nie ZL
FAU - Shi, Jian-Quan
AU  - Shi JQ
FAU - Zhao, Shan
AU  - Zhao S
FAU - Lu, Xiang
AU  - Lu X
FAU - Wang, Lian-Sheng
AU  - Wang LS
FAU - Yang, Zhi-Jian
AU  - Yang ZJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140505
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tea)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 8R1V1STN48 (Catechin)
RN  - BQM438CTEL (epigallocatechin gallate)
SB  - IM
MH  - Catechin/*analogs & derivatives/pharmacology
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Dose-Response Relationship, Drug
MH  - Human Umbilical Vein Endothelial Cells/*drug effects/*metabolism
MH  - Humans
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Structure-Activity Relationship
MH  - Tea/*chemistry
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors/pharmacology
EDAT- 2014/05/24 06:00
MHDA- 2015/04/15 06:00
CRDT- 2014/05/24 06:00
PHST- 2014/03/11 00:00 [accepted]
PHST- 2014/05/24 06:00 [entrez]
PHST- 2014/05/24 06:00 [pubmed]
PHST- 2015/04/15 06:00 [medline]
AID - 000358702 [pii]
AID - 10.1159/000358702 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2014;33(5):1349-58. doi: 10.1159/000358702. Epub 2014 May 
      5.