혈관내피세포에서 TNF-α 자극에 의해 유도되는 혈관염증에 대한 WK-38의 억제 효과
Inhibitory Effect of WK-38 on TNF-α Induced Vascular Inflammation in Human Umbilical Vein Endothelial Cells
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Vascular inflammation is an important event in the development of vascular diseases such as tumor progression and atherosclerosis. This study was to investigate the inhibitory effects of WK-38, a new herbal prescription for the treatment of atherosclerosis, on vascular inflammation in human umbilical vein endothelial cells (HUVEC). WK-38 is composed of Rhei Rhizoma, Magonoliae Cortex, Moutan Cortex Radicis. Pretreatment with WK-38 was significantly blocked TNF-α-induced expression level of cell adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), and endothelial cell selectin (E-selectin) in a dose-dependent manner. TNF-α-induced cell adhesion in co-cultured U937 and HUVEC was also blocked by pretreatment with WK-38. Moreover, WK-38 significantly suppressed p65 NF-κB translocation into the nucleus by TNF-α as well as the phosphorylation and degradation of IκB-α. In conclusion, the present data suggested that WK-38 could suppress TNF-α-induced vascular inflammatory process, though inhibition of NF-κB activation in HUVEC.
Abstract
Vascular inflammation is an important event in the development of vascular diseases such as tumor progression and atherosclerosis. This study was to investigate the inhibitory effects of WK-38, a new herbal prescription for the treatment of atherosclerosis, on vascular inflammation in human umbilical vein endothelial cells (HUVEC). WK-38 is composed of Rhei Rhizoma, Magonoliae Cortex, Moutan Cortex Radicis. Pretreatment with WK-38 was significantly blocked TNF-α-induced expression level of cell adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), and endothelial cell selectin (E-selectin) in a dose-dependent manner. TNF-α-induced cell adhesion in co-cultured U937 and HUVEC was also blocked by pretreatment with WK-38. Moreover, WK-38 significantly suppressed p65 NF-κB translocation into the nucleus by TNF-α as well as the phosphorylation and degradation of IκB-α. In conclusion, the present data suggested that WK-38 could suppress TNF-α-induced vascular inflammatory process, though inhibition of NF-κB activation in HUVEC.
참고문헌 (32)
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