Biochemical and Biophysical Research Communications
Regular ArticleHematein Inhibits Tumor Necrotic Factor-α-Induced Vascular Cell Adhesion Molecule-1 and NF-κB-Dependent Gene Expression in Human Vascular Endothelial Cells
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Combination of curcumin and luteolin synergistically inhibits TNF-α-induced vascular inflammation in human vascular cells and mice
2019, Journal of Nutritional BiochemistryCitation Excerpt :The critical roles of chemokines and adhesion molecules in the initiation and development of vascular inflammatory process and pathogenesis of CVDs have been well established [35,36]. For example, chemokine MCP-1 is essential for monocyte rolling, firm adhesion to ECs and the subsequent transmigration into vascular tissue [37,39,46] and adhesion molecules such as ICAM-1, VCAM-1, and E-selectin play a pivotal role in attracting, binding and transmigrating monocytes into sites of inflammation [38,47]. These have been confirmed by that mice lacking receptors for these molecules are less susceptible to vascular disease and have fewer monocytes in vascular lesions [39].
Pterostilbene exerts an anti-inflammatory effect via regulating endoplasmic reticulum stress in endothelial cells
2016, CytokineCitation Excerpt :Therefore, in this study, we chose TNF-α as an agent to induce inflammatory responses in endothelial cells. Additionally, IL-8 and MCP-1, the key chemokines that play regulatory roles in the interactions between monocytes and endothelial cells and in the migration of monocytes into vessels [26], were chosen as inflammatory markers. Adhesion molecules have also been identified as atherosclerotic inflammatory markers, including MMP9, ICAM1 and E-selectin [10,20].
Luteolin protects against vascular inflammation in mice and TNF-alpha-induced monocyte adhesion to endothelial cells via suppressing IKBα/NF-κB signaling pathway
2015, Journal of Nutritional BiochemistryCitation Excerpt :In addition to chemokines, adhesion molecules such as ICAM-1, VCAM-1 and E-selectin also play a pivotal role in attracting, binding and transmigrating monocytes into sites of inflammation [41]. In fact, these adhesion molecules are considered atherosclerotic inflammatory markers [42,43], which are increased in advanced human coronary atherosclerotic plaques as well as in experimental models of atherosclerosis [42,43]. In this study, our data showed that luteolin treatment remarkably suppressed TNF-α-induced expression of MCP-1, VCAM-1 and ICAM-1 in cultured ECs.
Sulforaphane reduces vascular inflammation in mice and prevents TNF-α-induced monocyte adhesion to primary endothelial cells through interfering with the NF-κB pathway
2014, Journal of Nutritional BiochemistryCitation Excerpt :Indeed, MCP-1 is found in human atheroma, and mice lacking a MCP-1 receptor are found to be less susceptible to atherosclerosis [44]. The adhesion molecules ICAM-1, VCAM-1 and E-selectin are known atherosclerotic inflammatory markers [45,46], which are largely increased in advanced human coronary atherosclerotic plaques, as well as in experimental models of atherosclerosis[45,46]. Also, these adhesion molecules are widely expressed in ECs.
Genistein inhibits TNF-α-induced endothelial inflammation through the protein kinase pathway A and improves vascular inflammation in C57BL/6 mice
2013, International Journal of CardiologyCitation Excerpt :Cytokines such as TNF-α induces the expression of adhesion molecules on the cell surface of ECs resulting in the adhesion and migration of monocytes to the subendothelial space [3]. The adhesion molecules such as ICAM-1, VCAM-1, and E-selectin have been suggested to be atherosclerotic inflammatory markers [59,60]. Indeed, previous studies have demonstrated increased expression of these endothelium-derived adhesion molecules in advanced human coronary atherosclerotic plaques as well as in experimental models of atherosclerosis [59,60].
4-O-methylgallic acid down-regulates endothelial adhesion molecule expression by inhibiting NF-κB-DNA-binding activity
2006, European Journal of Pharmacology
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