Resolvin E1

Resolvin E1 (RvE1), a potent endogenous pro-resolving mediator of inflammation, is derived from omega-3 fatty acid eicosapentaenoic acid (EPA). Resolvin E1 is endogenously biosynthesized from EPA in the presence of Aspirin during the spontaneous resolution phase of acute inflammation, where specific cell-cell interactions occur. Resolvin E1 possesses unique counterregulatory actions that inhibit polymorphonuclear leukocyte (PMN) transendothelial migration. Resolvin E1 also acts as a potent inhibitor of leukocyte infiltration, dendritic cell migration, and IL-12 production^[1][2]. In Vitro: Resolvin E1 (0.1-100 nM) gives concentration-dependent inhibition of TNF-α–induced NF-κB activation with an EC50 of ∼1.0 nM in ChemR23-transfected cells. Resolvin E1 (100 nM) increases phosphorylation of extracellular signal-regulated kinase (ERK) mitogen-activated protein (MAP) kinase both in peripheral blood monocytes and HEK-ChemR23 cells^[2]. Resolvin E1 specifically interacts with the LTB₄ receptor BLT1 on neutrophils and ChemR23 on monocytes to regulate leukocytes during inflammation. Resolvin E1 also stimulates the uptake and clearance of local cytokine^[3]. In Vivo: Resolvin E1 (1.0 μg per mouse; 50 μg/kg; i.p.; on days -8, -1, and 0) protects mice from TNBS (2,4,6-trinitrobenzene sulfonic acid) colitis^[1].