Bisacurone inhibits adhesion of inflammatory monocytes or cancer cells to endothelial cells through down-regulation of VCAM-1 expression
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- Bisacurone inhibits adhesion of inflammatory monocytes or cancer cells to endothelial cells through down-regulation of VCAM-1 expression
- D I Sun; I T Nizamutdinova; Y M Kim; X F Cai; Jung Joon Lee; S S Kang; Y S Kim; K M Kang; G Y Chai; K C Chang; H J Kim
- Bibliographic Citation
- International Immunopharmacology, vol. 8, no. 9, pp. 1272-1281
- Publication Year
- Bisacurone, one of the active compounds of the traditionally used indigenous herb Curcuma longa Linne (Zingiberaceae), has anti-oxidant, anti-inflammatory, and anti-metastatic activities. We studied how the level of vascular cell adhesion molecule-1 (VCAM-1), one of the key molecules in the development of atherosclerosis as well as carcinogenesis and metastasis, might be affected by bisacurone in tumor necrosis factor-alpha (TNF-α)-activated human umbilical vein endothelial cells (HUVECs). Bisacurone dose-dependently inhibited TNF-α-mediated expression of VCAM-1. It showed significant suppressive effect on ROS generation in response to TNF-α stimulation and it blocked nuclear factor-kappa B (NF-κB) p65 translocation into the nucleus and phosphorylation of inhibitory factor κBα (IκBα). It also inhibited phosphorylation of Akt and PKC, which are upstream in the regulation of VCAM-1 by TNF-α. Furthermore, bisacurone decreased U937 monocyte and human oral cancer cell (Hep-2, QLL-I, SCC-15) adhesion to HUVECs stimulated by TNF-α, suggesting that it may inhibit the binding of these cells by regulating the expression of critical adhesion molecules by TNF-α. Thus, bisacurone may be beneficial in the treatment of inflammatory diseases, such as atherosclerosis, where inflammatory monocytes are involved in their pathology, and, moreover, in the development of tumors.
- Bisacurone; Inflammatory disease; Metastasis; NF-kappa B; Reactive oxygen species; Vascular cell adhesion molecule-1
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- 1. Journal Articles > Journal Articles
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