Chlorophyll-Related Compounds Inhibit Cell Adhesion and Inflammation in Human Aortic Cells

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Title:	Chlorophyll-Related Compounds Inhibit Cell Adhesion and Inflammation in Human Aortic Cells
Authors:	Lin, KH (Lin, Kuan-Hung) Hsu, CY (Hsu, Ching-Yun) Huang, YP (Huang, Ya-Ping) Lai, JY (Lai, Jun-You) Hsieh, WB (Hsieh, Wen-Bin) Huang, MY (Huang, Meng-Yuan) Yang, CM (Yang, Chi-Ming) Chao, PY (Chao, Pi-Yu)
Contributors:	Grad Inst Biotechnol
Keywords:	anti-inflammatory chlorophylls human aortic endothelial cells human aortic smooth muscle cells
Date:	2013-10-01
Issue Date:	2014-02-24 15:26:36 (UTC+8)
Abstract:	The objectives of this study were to investigate the effects of chlorophyll-related compounds (CRCs) and chlorophyll (Chl) a+b on inflammation in human aortic endothelial cells. Adhesion molecule expression and interleukin (IL)-8, nuclear factor (NF)-B p65 protein, and NF-B and activator protein (AP)-1 DNA binding were assessed. The effects of CRCs on inflammatory signaling pathways of signal transducers and activators of transcription 3 (STAT3) and mothers against decapentaplegic homolog 4, respectively induced by IL-6 and transforming growth factor (TGF)-, in human aortic smooth muscle cells cultured in vitro were also investigated. HAECs were pretreated with 10 M of CRCs, Chl a+b, and aspirin (Asp) for 18h followed by tumor necrosis factor (TNF)- (2ng/mL) for 6h, and U937 cell adhesion was determined. TNF--induced monocyte-endothelial cell adhesion was significantly inhibited by CRCs. Moreover, CRCs and Chl a+b significantly attenuated vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and IL-8 expressions. Treatments also significantly decreased in NF-B expression, DNA binding, and AP-1 DNA binding by CRCs and Asp. Thus, CRCs exert anti-inflammatory effects through modulation of NF-B and AP-1 signaling. Ten micromoles of CRCs and Asp upregulated the expression of mothers against decapentaplegic homolog 4 (Drosophila) (SMAD4) in the TGF- receptor signaling pathway, and SMAD3/4 transcription activity was also increased. Ten micromoles of CRCs were able to potently inhibit STAT3-binding activity by repressing IL-6-induced STAT3 expression. Our results provide a potential mechanism that explains the anti-inflammatory activities of these CRCs.
Relation:	JOURNAL OF MEDICINAL FOOD Volume: 16 Issue: 10 Pages: 886-898
Appears in Collections:	[Graduate Institute of Biotechnology ] journal articles

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