Abstract
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.
Highlights
Cardiovascular disease (CVD) has a high mortality rate worldwide and has become a critical health concern, in consideration of population aging
The levels of IL-8, intercellular adhesion molecule-1 (ICAM-1), and monocyte chemoattractant protein- (MCP-)1 increased significantly after the application of cyclic strain for 24 h compared with static control cells
We evaluated the effect of cafestol on the secretion of the inflammatory proteins MCP-1, ICAM-1, and IL-8 by using enzyme-linked immunosorbent assay (ELISA)
Summary
Cardiovascular disease (CVD) has a high mortality rate worldwide and has become a critical health concern, in consideration of population aging. Research evaluating mechanisms underlying the favorable relationship between coffee consumption and reduction in risk factors for CVD is extremely limited. Endothelial inflammation is Oxidative Medicine and Cellular Longevity associated with a high risk of adverse cardiovascular events [2, 3] and plays a key role in the development of CVD [4]. Several natural compounds present in coffee, such as phenolic compounds, flavonoids, and caffeic acid derivatives, have been reported to possess an anti-inflammatory property [5]. This anti-inflammatory property is likely responsible for the favorable relationship between coffee consumption and a low CVD mortality rate [6, 7]. The effect of cafestol on vascular endothelial cells remains to be clarified
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