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Allicin Reduces Adhesion Molecules and NO Production Induced by gamma irradiation in Human Endothelial Cells
Immune Network ; : 6-11, 2002.
Artículo en Coreano | WPRIM | ID: wpr-213060
ABSTRACT

BACKGROUND:

Inflammation is a frequent reaction following therapeutic irradiation. Since the upregulation of adhesion molecules on endothelial cell surface is known to be associated with inflammation, the expression of adhesion molecules is an important therapeutic target.

METHODS:

Treatment of human umbilical endothelial cells (HUVECs) with gamma irradiation (gamma R) induces the expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Changes in the expression of these proteins on gamma irradiated HUVECs which had been treated previously with allicin were measured by ELISA.

RESULTS:

In the present study, we demonstrate that allicin inhibits the gamma R induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose-dependent manner. Allicin was also found to inhibit thegamma R induced production of nitric oxide (NO).

CONCLUSION:

These data suggest that allicin has a therapeutic potential for the treatment of various inflammatory disorders associated with increase numbers of endothelial leukocyte adhesion molecules.
Asunto(s)

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Ensayo de Inmunoadsorción Enzimática / Moléculas de Adhesión Celular / Regulación hacia Arriba / Molécula 1 de Adhesión Intercelular / Molécula 1 de Adhesión Celular Vascular / Selectina E / Células Endoteliales / Inflamación / Óxido Nítrico Límite: Humanos Idioma: Coreano Revista: Immune Network Año: 2002 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Ensayo de Inmunoadsorción Enzimática / Moléculas de Adhesión Celular / Regulación hacia Arriba / Molécula 1 de Adhesión Intercelular / Molécula 1 de Adhesión Celular Vascular / Selectina E / Células Endoteliales / Inflamación / Óxido Nítrico Límite: Humanos Idioma: Coreano Revista: Immune Network Año: 2002 Tipo del documento: Artículo