Inhibition of adhesion molecules expression by allicin in TNF‐α‐ and LPS‐treated MOVAS via downregulation of NF‐κB

Allicin is a precursor of a number of secondary products formed in garlic preparations. Since the upregulation of adhesion molecules in response to numerous inducing factors is associated with inflammation, interfering with the expression of adhesion molecules may be an important therapeutic target of inflammatory diseases. We examined the effect of allicin on the expression of adhesion molecules induced by TNF‐α or LPS in cultured mouse vascular smooth muscle cells (MOVAS) by ELISA, Western blot and Luciferase analysis, respectively. MOVAS were pretreated for 20 h with allicin (0.01‐1 μg/ml) and then exposed to TNF‐α or LPS for 4 and 8 h to measure the expression of E‐selectin, VCAM‐1 and ICAM‐1, respectively. Allicin significantly inhibited surface expression of adhesion molecules in a dose dependent manner. Specifically, the most significant reduction was observed in ICAM‐1 expression. In addition, allicin treatment resulted in the decrease of NF‐κB activation, whereas phosphorylation of AKT and ERK induced by LPS but not TNF‐α was inhibited. These results suggest that allicin downregulates TNF‐α‐ or LPS‐induced adhesion molecules expression via inhibition of NF‐κB activity and LPS‐mediated induction of adhesion molecules by inhibiting AKT and ERK signaling. Moreover, the data indicate that allicin may be considered in therapeutic strategies for the management of vascular inflammatory diseases