Vascular endothelial growth factor (VEGF) is well known as a significant angiogenic factor, and also functions as a proinflammatory cytokine, which induces adhesion of leukocyte to endothelial cells in inflammation reaction. In this study, we show that ganglioside GM3 inhibits the VEGF-induced expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) through activation of nuclear factor-κB (NF-κB) via protein kinase B (AKT) signaling in human umbilical vein endothelial cells (HUVECs), relating with leukocyte recruitment to endothelial cells under inflammatory conditions. In addition, ganglioside GM3 significantly reduced the monocyte adhesion to HUVECs as determined by the monolayer cell adhesion assay. Furthermore, in VEGF-injected mice for the inflammatory condition, ganglioside GM3 markedly decreased the expression of ICAM-1 and VCAM-1 in vein tissues. These results suggest that ganglioside GM3 has an anti-inflammatory role by suppressing the expression of inflammatory-related molecules during in vitro and in vivo inflammation.
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