Oleylethanolamide (Synonyms: Oleic Acid Ethanolamide, OEA) |
Catalog No.GC16103 |
L'oléyléthanolamide est un PPAR-α endogène de haute affinité ; agoniste, qui joue un rÔle important dans le traitement de l'obésité et de l'artériosclérose.
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Cas No.: 111-58-0
Sample solution is provided at 25 µL, 10mM.
Oleoylethanolamide is a high affinity endogenous PPAR-α agonist, which plays an important role in the treatment of obesity and arteriosclerosis.
Oleoylethanolamide (OEA), an endogenous PPAR-α ligand, attenuates liver fibrosis targeting hepatic stellate cells. Oleoylethanolamide suppresses TGF-β1 induced hepatic stellate cells (HSCs) activation in vitro via PPAR-α. To assess the impact of Oleoylethanolamide on HSCs activation, the expression levels of α-SMA and Col1a in TGF-β1-stimulated HSCs are examined by qPCR. The mRNA levels of α-SMA and Col1a are markedly induced in the group of CFSC cells with TGF-β1 (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 α-SMA, the marker of HSC activation. The inhibitory effects of Oleoylethanolamide on HSCs activation are completely blocked by PPAR-α antagonist MK886 (10 μM). Moreover, the mRNA and protein expression levels of PPAR-α are down-regulated with TGF-β1 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-β1 stimulation, consistent with the observed effects on HSC activation, while Oleoylethanolamide (10 μM) reduces the phosphorylation of Smad2/3 in CFSC simulated with TGF-β1[1].
Oleoylethanolamide (OEA) can significantly suppress the pro-fibrotic cytokine TGF-β1 negatively regulate genes in the TGF-β1 signaling pathway (α-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].
References:
[1]. Chen L, et al. Oleoylethanolamide, an endogenous PPAR-α ligand, attenuates liver fibrosis targeting hepatic stellate cells. Oncotarget. 2015 Dec 15;6(40):42530-40
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