Inhibitory Effects of Allicin on TNF-α-induced ICAM-1 Expression is Associated with Catalase
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Allicin, a garlic componente, is believed to provide protection against various diseases including inflammation. Since interactions of the cell adhesion molecules are known to play important roles in mediating inflammation, inhibiting adhesion protein upregulation is a possible therapeutic target. In this study, we demonstrate that TNF-α- and catalase-induced expression of ICAM-1 on human lung epithelial cells (A549) in a dose-dependent manner and catalase expression and activity were also increased in TNF-α-treated cells. Treatment of the TNF-α-treated cells with catalase inhibitor 3-amino-1,2,4-triazole resulted in a significant decreased the level of ICAM-1. These data suggest that induction of ICAM-1 expression by TNF-α is associated with catalase. In addition, allicin was found to inhibit the TNF-α induced expression of ICAM-1 on the A549 cells. This compound also inhibited the production of catalase induced by TNF-α, which suggests that the inhibition of ICAM-1 expression by allicin may be due to the modulated production of catalase.
Abstract
Allicin, a garlic componente, is believed to provide protection against various diseases including inflammation. Since interactions of the cell adhesion molecules are known to play important roles in mediating inflammation, inhibiting adhesion protein upregulation is a possible therapeutic target. In this study, we demonstrate that TNF-α- and catalase-induced expression of ICAM-1 on human lung epithelial cells (A549) in a dose-dependent manner and catalase expression and activity were also increased in TNF-α-treated cells. Treatment of the TNF-α-treated cells with catalase inhibitor 3-amino-1,2,4-triazole resulted in a significant decreased the level of ICAM-1. These data suggest that induction of ICAM-1 expression by TNF-α is associated with catalase. In addition, allicin was found to inhibit the TNF-α induced expression of ICAM-1 on the A549 cells. This compound also inhibited the production of catalase induced by TNF-α, which suggests that the inhibition of ICAM-1 expression by allicin may be due to the modulated production of catalase.
참고문헌 (23)
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