111-58-0
基本信息
油酰乙醇胺
油酰胺 MEA
油酰单乙醇胺
ODA
OLEIC ACID-2,6-DIISOPROPYL ANILIDE
N-(2-hydroxyethyl)-,(Z)-9-Octadecenamide
Oleoylmonoethanolamide
OLEAMIDE MEA
9-Octadecenamide, N-(2-hydroxyethyl)-, (9Z)-
(Z)-N-(2-hydroxyethyl)octadec-9-enamide
LSUREMONOETHANOLAMID
Oleyl monoethanolamide
N-(2-Hydroxyethyl)oleamide
N-(cis-9-Octadecenoyl)ethanolamine
N-Oleoylethanolamine
OEA
N-(cis-9-Octadecenoyl)ethanolamine, N-(Hydroxyethyl)oleamide, OEA, oleoylethanolamide
(Z)-N-(2-Hydroxyethyl)-9-octadecenamide
AM-3101
N-(2-Hydroxyethyl)oleic amide
物理化学性质
| 熔点 | 63-64 °C |
| 沸点 | 496.4±38.0 °C(Predicted) |
| 密度 | 0.915±0.06 g/cm3(Predicted) |
| 储存条件 | −20°C |
| 储存条件 | -20°C |
| 溶解度 | 可溶于DMSO（高达25mg/ml）或乙醇（高达35mg/ml） |
| 酸度系数(pKa) | 14.49±0.10(Predicted) |
| 形态 | 白色固体 |
| 颜色 | 白色 |
| 稳定性 | Stable for 2 years from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 1 month. |
| InChI | InChI=1S/C20H39NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-20(23)21-18-19-22/h9-10,22H,2-8,11-19H2,1H3,(H,21,23)/b10-9- |
| InChIKey | BOWVQLFMWHZBEF-KTKRTIGZSA-N |
| SMILES | C(NCCO)(=O)CCCCCCC/C=C\CCCCCCCC |
| LogP | 6.406 (est) |
| CAS 数据库 | 111-58-0(CAS DataBase Reference) |
| EPA化学物质信息 | 9-Octadecenamide, N-(2-hydroxyethyl)-, (9Z)- (111-58-0) |
安全数据
| 危险性符号(GHS) |   GHS09,GHS05 |
| 警示词 | 危险 |
| 危险性描述 | H315-H411-H318 |
| 防范说明 | P264-P280-P302+P352-P321-P332+P313-P362-P280-P305+P351+P338-P310 |
| 危险品标志 | Xi |
| 危险类别码 | 36/37/38 |
| 危险类别码 | R36/37/38 |
| 安全说明 | 26-36 |
| 安全说明 | S26-S36 |
| WGK Germany | 2 |
| WGK Germany | 2 |
| 危险等级 | IRRITANT |
常见问题列表
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Human Endogenous Metabolite
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PPAR-α
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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.
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).