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

Jung Joo Hong; Jae Hoon Choi; Sei Ryang Oh; Hyeong Kyu Lee; Jae Hak Park; Kun Yeong Lee; Jung Jae Kim; Tae Sook Jeong; Goo Taeg Oh

doi:10.1016/S0014-5793(01)02379-1

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

Jung Joo Hong, Jae Hoon Choi, Sei Ryang Oh, Hyeong Kyu Lee, Jae Hak Park, Kun Yeong Lee, Jung Jae Kim, Tae Sook Jeong, Goo Taeg Oh

Department of Life Science

Research output: Contribution to journal › Article › peer-review

60 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	142-147
Number of pages	6
Journal	FEBS Letters
Volume	495
Issue number	3
DOIs	https://doi.org/10.1016/S0014-5793(01)02379-1
State	Published - 27 Apr 2001

Bibliographical note

Funding Information:
We wish to thank Dr. Nobuyo Maeda (UNC-Chapel Hill, NC, USA) for helpful comments and suggestions, Ju-Ryoung Kim for FPLC analysis, Myoung-Soo Kim, Seong-Kyu Kim for their technical assistance, and Philip McElroy for the English revision. This work was financially supported by the Molecular Medicine Research Group Program (99-J03-01-01-A-05) from MOST and the SGRP/HTD Program (298045-3) from ARPC, Korea.

Keywords

Agastache rugosa
Atherosclerosis
Macrophage
Nuclear factor-κB
Tilianin
Vascular cell adhesion molecule-1

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10.1016/S0014-5793(01)02379-1

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title = "Inhibition of cytokine-induced vascular cell adhesion molecule-1 expression; possible mechanism for anti-atherogenic effect of Agastache rugosa",

abstract = "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.",

keywords = "Agastache rugosa, Atherosclerosis, Macrophage, Nuclear factor-κB, Tilianin, Vascular cell adhesion molecule-1",

author = "Hong, {Jung Joo} and Choi, {Jae Hoon} and Oh, {Sei Ryang} and Lee, {Hyeong Kyu} and Park, {Jae Hak} and Lee, {Kun Yeong} and Kim, {Jung Jae} and Jeong, {Tae Sook} and Oh, {Goo Taeg}",

note = "Funding Information: We wish to thank Dr. Nobuyo Maeda (UNC-Chapel Hill, NC, USA) for helpful comments and suggestions, Ju-Ryoung Kim for FPLC analysis, Myoung-Soo Kim, Seong-Kyu Kim for their technical assistance, and Philip McElroy for the English revision. This work was financially supported by the Molecular Medicine Research Group Program (99-J03-01-01-A-05) from MOST and the SGRP/HTD Program (298045-3) from ARPC, Korea.",

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doi = "10.1016/S0014-5793(01)02379-1",

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AU - Choi, Jae Hoon

AU - Oh, Sei Ryang

AU - Lee, Hyeong Kyu

AU - Park, Jae Hak

AU - Lee, Kun Yeong

AU - Kim, Jung Jae

AU - Jeong, Tae Sook

AU - Oh, Goo Taeg

N1 - Funding Information: We wish to thank Dr. Nobuyo Maeda (UNC-Chapel Hill, NC, USA) for helpful comments and suggestions, Ju-Ryoung Kim for FPLC analysis, Myoung-Soo Kim, Seong-Kyu Kim for their technical assistance, and Philip McElroy for the English revision. This work was financially supported by the Molecular Medicine Research Group Program (99-J03-01-01-A-05) from MOST and the SGRP/HTD Program (298045-3) from ARPC, Korea.

PY - 2001/4/27

Y1 - 2001/4/27

N2 - 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.

AB - 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.

KW - Agastache rugosa

KW - Atherosclerosis

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KW - Nuclear factor-κB

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

Abstract

Bibliographical note

Keywords

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