Inhibition of cytokine‐induced vascular cell adhesion molecule‐1 expression; possible mechanism for anti‐atherogenic effect of Agastache rugosa

FEBS Letters

Oh, Sei-Ryang⁴  Jeong, Tae-Sook³  Oh, Goo Taeg¹  Hong, Jung-Joo¹  Choi, Jae-Hoon¹  Park, Jae-Hak²  Kim, Jung-Jae¹  Lee, Hyeong-Kyu⁴  Lee, Kun-Yeong¹ 

[1] Genetic Resources Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), P.O. Box 115, Yusong, Taejon 305-600, South Korea;College of Veterinary Medicine, Seoul National University, Suwon 441-744, South Korea;Cardiovascular Research Laboratory, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Yusong, Taejon 305-600, South Korea;Immunomodulator Research Laboratory, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Yusong, Taejon 305-600, South Korea

关键词: Atherosclerosis;    Tilianin;    Vascular cell adhesion molecule-1;    Macrophage;    Nuclear factor-κB;    Agastache rugosa;   

DOI  :  10.1016/S0014-5793(01)02379-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) play an important role during the early stages of atherogenesis. Agastache rugosa has an anti-atherogenic effect in low density lipoprotein receptor −/− mice. Moreover, A. rugosa reduced macrophage infiltration and VCAM-1 expression has been localized in aortic endothelium that overlies early foam cell lesions. This study ascertained that tilianin (100 μM), a major component of A. rugosa, inhibits the tumor necrotic factor-α (TNF-α)-induced expression of VCAM-1 by 74% in cultured human umbilical vein endothelial cells (HUVECs). Also, tilianin (100 μM) reduced TNF-α-induced activation of nuclear factor-κB in HUVECs.

【 授权许可】

Unknown