Journal of Physiology & Pathology in Korean Medicine (동의생리병리학회지)

The Physiological Society of Korean Medicine and The Society of Pathology in Korean Medicine (대한동의생리학회·한의병리학회)
권호 표지

Inhibitory Effect of WK-38 on TNF-$\alpha$ Induced Vascular Inflammation in Human Umbilical Vein Endothelial Cells

혈관내피세포에서 TNF-$\alpha$ 자극에 의해 유도되는 혈관염증에 대한 WK-38의 억제 효과

  • Hwang, Sun-Mi (Professional Graduate School of Oriental Medicine, Wonkwang University) ;
  • Lee, Yun-Jung (Professional Graduate School of Oriental Medicine, Wonkwang University) ;
  • Kim, Eun-Ju (Professional Graduate School of Oriental Medicine, Wonkwang University) ;
  • Yoon, Jung-Joo (Professional Graduate School of Oriental Medicine, Wonkwang University) ;
  • Lee, Hyeok (Professional Graduate School of Oriental Medicine, Wonkwang University) ;
  • Kang, Dae-Gill (Professional Graduate School of Oriental Medicine, Wonkwang University) ;
  • Lee, Ho-Sub (Professional Graduate School of Oriental Medicine, Wonkwang University)
  • 황선미 (원광대학교 한의학전문대학원) ;
  • 이윤정 (원광대학교 한의학전문대학원) ;
  • 김은주 (원광대학교 한의학전문대학원) ;
  • 윤정주 (원광대학교 한의학전문대학원) ;
  • 이혁 (원광대학교 한의학전문대학원) ;
  • 강대길 (원광대학교 한의학전문대학원) ;
  • 이호섭 (원광대학교 한의학전문대학원)
  • Published : 2009.10.25
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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 Cortez Radicis. Pretreatment with WK-38 was significantly blocked TNF-$\alpha$-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-$\alpha$-induced cell adhesion in co-cultured U937 and HUVEC was also blocked by pretreatment with WK-38. Moreover, WK-38 significantly suppressed p65 NF-${\kappa}B$ translocation into the nucleus by TNF-$\alpha$ as well as the phosphorylation and degradation of $I{\kappa}B-{\alpha}$. In conclusion, the present data suggested that WK-38 could suppress TNF-$\alpha$-induced vascular inflammatory process, though inhibition of NF-${\kappa}B$ activation in HUVEC.

Keywords

References

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