PMID- 21491909
OWN - NLM
STAT- MEDLINE
DCOM- 20110928
LR  - 20121115
IS  - 1520-5118 (Electronic)
IS  - 0021-8561 (Linking)
VI  - 59
IP  - 10
DP  - 2011 May 25
TI  - Andrographolide inhibits ICAM-1 expression and NF-kappaB activation in TNF-alpha-treated 
      EA.hy926 cells.
PG  - 5263-71
LID - 10.1021/jf104003y [doi]
AB  - Several lines of evidence indicate that inflammation and endothelial cell 
      dysfunction are important initiating events in atherosclerosis. Tumor necrosis 
      factor-alpha (TNF-alpha), a pro-inflammatory cytokine, induces the expression of cell 
      adhesion molecules and results in monocyte adherence and atheromatous plaque 
      formation. Andrographolide (AP) is a major bioactive diterpene lactone in 
      Andrographis paniculata that has anti-inflammatory activity. A previous study 
      demonstrated the role of heme oxygenase 1 (HO-1) in the inhibition of 
      TNF-alpha-induced ICAM-1 expression by AP. The present study investigated the effect 
      of AP on the IKK/NF-kappaB signaling pathway, which mediates TNF-alpha-induced ICAM-1 
      expression in EA.hy926 cells. Similar to the previous study, AP inhibited 
      TNF-alpha-induced ICAM-1 mRNA and protein levels, its expression on the cell surface, 
      and subsequent adhesion of HL-60 cells to EA.hy926 cells. AP inhibited 
      TNF-alpha-induced kappaB inhibitor (IkappaB) kinase (IKK) and IkappaBalpha activation, p65 nuclear 
      translocation, NF-kappaB and DNA binding activity, and promoter activity of ICAM-1. 
      Although AP increased the intracellular cAMP concentration and induced the 
      phosphorylation of cAMP response element-binding protein (CREB), knocking down 
      CREB protein expression by transfecting the cells with CREB-specific small 
      interfering RNA did not relieve the inhibition of ICAM-1 expression by AP. Taken 
      together, these results suggest that AP down-regulates TNF-alpha-induced ICAM-1 
      expression at least in part via attenuation of activation of NF-kappaB in EA.hy926 
      cells rather than through activation of CREB. The results suggest that AP may 
      have potential as a cardiovascular-protective agent.
FAU - Chao, Che-Yi
AU  - Chao CY
AD  - Department of Health and Nutritional Biotechnology, Asia University, Taichung, 
      Taiwan.
FAU - Lii, Chong-Kuei
AU  - Lii CK
FAU - Tsai, I-Ting
AU  - Tsai IT
FAU - Li, Chien-Chun
AU  - Li CC
FAU - Liu, Kai-Li
AU  - Liu KL
FAU - Tsai, Chia-Wen
AU  - Tsai CW
FAU - Chen, Haw-Wen
AU  - Chen HW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110426
PL  - United States
TA  - J Agric Food Chem
JT  - Journal of agricultural and food chemistry
JID - 0374755
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Diterpenes)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 410105JHGR (andrographolide)
SB  - IM
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cardiovascular Diseases/prevention & control
MH  - Cell Adhesion/drug effects
MH  - Cell Line
MH  - Diterpenes/*pharmacology
MH  - Endothelial Cells/drug effects/physiology
MH  - Gene Expression/*drug effects
MH  - HL-60 Cells
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/analysis/*genetics
MH  - NF-kappa B/*antagonists & inhibitors
MH  - RNA, Messenger/analysis
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 2011/04/16 06:00
MHDA- 2011/09/29 06:00
CRDT- 2011/04/16 06:00
PHST- 2011/04/16 06:00 [entrez]
PHST- 2011/04/16 06:00 [pubmed]
PHST- 2011/09/29 06:00 [medline]
AID - 10.1021/jf104003y [doi]
PST - ppublish
SO  - J Agric Food Chem. 2011 May 25;59(10):5263-71. doi: 10.1021/jf104003y. Epub 2011 
      Apr 26.