KMID : 1161420130160100886
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Journal of Medicinal Food 2013 Volume.16 No. 10 p.886 ~ p.898
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Chlorophyll-Related Compounds Inhibit Cell Adhesion and Inflammation in Human Aortic Cells
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Lin Kuan-Hung
Hsu Ching-Yun Huang Ya-Ping Lai Jun-You Hsieh Wen-Bin Huang Meng-Yuan Yang Chi-Ming Chao Pi-Yu
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Abstract
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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)-¥êB p65 protein, and NF-¥êB 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)-¥â, in human aortic smooth muscle cells cultured in vitro were also investigated. HAECs were pretreated with 10 ¥ìM of CRCs, Chl a+b, and aspirin (Asp) for 18?h followed by tumor necrosis factor (TNF)-¥á (2?ng/mL) for 6?h, and U937 cell adhesion was determined. TNF-¥á?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-¥êB expression, DNA binding, and AP-1 DNA binding by CRCs and Asp. Thus, CRCs exert anti-inflammatory effects through modulation of NF-¥êB and AP-1 signaling. Ten micromoles of CRCs and Asp upregulated the expression of mothers against decapentaplegic homolog 4 (Drosophila) (SMAD4) in the TGF-¥â 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.
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KEYWORD
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anti-inflammatory, chlorophylls, human aortic endothelial cells, human aortic smooth muscle cells
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