Academic Journal
Cafestol Inhibits Cyclic‐Strain‐Induced Interleukin‐8, Intercellular Adhesion Molecule‐1, and Monocyte Chemoattractant Protein‐1 Production in Vascular Endothelial Cells
العنوان: | Cafestol Inhibits Cyclic‐Strain‐Induced Interleukin‐8, Intercellular Adhesion Molecule‐1, and Monocyte Chemoattractant Protein‐1 Production in Vascular Endothelial Cells |
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المؤلفون: | Hao, Wen-Rui, Sung, Li-Chin, Chen, Chun-Chao, Chen, Po-Yuan, Cheng, Tzu-Hurng, Chao, Hung-Hsing, Liu, Ju-Chi, Chen, Jin-Jer |
المساهمون: | Valencia, Débora Villaño, Shin Kong Wu Ho-Su Memorial Hospital, Ministry of Science and Technology |
المصدر: | Oxidative Medicine and Cellular Longevity ; volume 2018, issue 1 ; ISSN 1942-0900 1942-0994 |
بيانات النشر: | Wiley |
سنة النشر: | 2018 |
المجموعة: | Wiley Online Library (Open Access Articles via Crossref) |
الوصف: | Moderate coffee consumption is inversely associated with cardiovascular disease mortality; however, mechanisms underlying this causal effect remain unclear. Cafestol, a diterpene found in coffee, has various properties, including an anti‐inflammatory property. This study investigated the effect of cafestol on cyclic‐strain‐induced inflammatory molecule secretion in vascular endothelial cells. Cells were cultured under static or cyclic strain conditions, and the secretion of inflammatory molecules was determined using enzyme‐linked immunosorbent assay. The effects of cafestol on mitogen‐activated protein kinases (MAPK), heme oxygenase‐1 (HO‐1), and sirtuin 1 (Sirt1) signaling pathways were examined using Western blotting and specific inhibitors. Cafestol attenuated cyclic‐strain‐stimulated intercellular adhesion molecule‐1 (ICAM‐1), monocyte chemoattractant protein‐ (MCP‐) 1, and interleukin‐ (IL‐) 8 secretion. Cafestol inhibited the cyclic‐strain‐induced phosphorylation of extracellular signal‐regulated kinase and p38 MAPK. By contrast, cafestol upregulated cyclic‐strain‐induced HO‐1 and Sirt1 expression. The addition of zinc protoporphyrin IX, sirtinol, or Sirt1 silencing (transfected with Sirt1 siRNA) significantly attenuated cafestol‐mediated modulatory effects on cyclic‐strain‐stimulated ICAM‐1, MCP‐1, and IL‐8 secretion. This is the first study to report that cafestol inhibited cyclic‐strain‐induced inflammatory molecule secretion, possibly through the activation of HO‐1 and Sirt1 in endothelial cells. The results provide valuable insights into molecular pathways that may contribute to the effects of cafestol. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
DOI: | 10.1155/2018/7861518 |
الاتاحة: | http://dx.doi.org/10.1155/2018/7861518 http://downloads.hindawi.com/journals/omcl/2018/7861518.pdf http://downloads.hindawi.com/journals/omcl/2018/7861518.xml https://onlinelibrary.wiley.com/doi/pdf/10.1155/2018/7861518 |
Rights: | http://creativecommons.org/licenses/by/4.0/ |
رقم الانضمام: | edsbas.DE9EDF4F |
قاعدة البيانات: | BASE |
DOI: | 10.1155/2018/7861518 |
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