Oleoylethanolamide

111-58-0

C20H39NO2

H2O : < 0.1 mg/mL (insoluble); DMSO : 20.83 mg/mL (63.99 mM; Need ultrasonic)

Cell Cycle/DNA Damage; Metabolic Enzyme/Protease

Oleoylethanolamide is a high affinity endogenous PPAR-alpha agonist, which plays an important role in the treatment of obesity and arteriosclerosis. IC50 & Target: PPAR-alpha^[1] In Vitro: Oleoylethanolamide (OEA), an endogenous PPAR-alpha ligand, attenuates liver fibrosis targeting hepatic stellate cells. Oleoylethanolamide suppresses TGF-beta1 induced hepatic stellate cells (HSCs) activation in vitro via PPAR-alpha. To assess the impact of Oleoylethanolamide on HSCs activation, the expression levels of alpha-SMA and Col1a in TGF-beta1-stimulated HSCs are examined by qPCR. The mRNA levels of alpha-SMA and Col1a are markedly induced in the group of CFSC cells with TGF-beta1 (5 ng/mL) stimulation for 48h, while the mRNA levels are suppressed when treated with Oleoylethanolamide in a dose-dependent manner. Immunofluorescence and western blot results show that Oleoylethanolamide treatment dose-dependently inhibits the protein expression of alpha-SMA, the marker of HSC activation. The inhibitory effects of Oleoylethanolamide on HSCs activation are completely blocked by PPAR-alpha antagonist MK886 (10 uM). Moreover, the mRNA and protein expression levels of PPAR-alpha are down-regulated with TGF-beta1 stimulation, while Oleoylethanolamide treatment restores these changes in dose-dependent manner. In addition, the phosphorylation of Smad 2/3 is upregulated in the presence of TGF-beta1 stimulation, consistent with the observed effects on HSC activation, while Oleoylethanolamide (10 uM) reduces the phosphorylation of Smad2/3 in CFSC simulated with TGF-beta1^[1]. In Vivo: Oleoylethanolamide (OEA) can significantly suppress the pro-fibrotic cytokine TGF-beta1 negatively regulate genes in the TGF-beta1 signaling pathway (alpha-SMA, collagen 1a, and collagen 3a) in mice models of hepatic fibrosis. Treatment with Oleoylethanolamide (5 mg/kg/day, intraperitoneal injection, i.p.) significantly attenuates the progress of liver fibrosis in both two experimental animal models by blocking the activation of hepatic stellate cells (HSCs)^[1].