Is suppression of Toll-like receptor 4 activation by caffeic acid phenethyl ester mediated by interference of LPS binding to MD2?
Our results show a novel mechanism for anti-inflammatory activity of CAPE to prevent TLR4 activation by interfering with interaction between ligand (LPS) and receptor complex (TLR4/MD2). These further provide beneficial information for the development of therapeutic strategies to prevent chronic inflammatory diseases.
Our findings suggest that blockade of RAS decreases tumor proliferation and metastatic capacity of RCC in this experimental model.