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https://irlib.pccu.edu.tw/handle/987654321/26707
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| 題名: | Chlorophyll-Related Compounds Inhibit Cell Adhesion and Inflammation in Human Aortic Cells |
| 作者: | 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) |
| 貢獻者: | Grad Inst Biotechnol |
| 關鍵詞: | anti-inflammatory
chlorophylls
human aortic endothelial cells
human aortic smooth muscle cells |
| 日期: | 2013-10-01 |
| 上傳時間: | 2014-02-24 15:26:36 (UTC+8) |
| 摘要: | 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. |
| 關聯: | JOURNAL OF MEDICINAL FOOD Volume: 16 Issue: 10 Pages: 886-898 |
| 顯示於類別: | [生物科技研究所 ] 期刊論文
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