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.
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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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Cell experiment: |
CFSC, HSC cell lines are first obtained from cirrhotic rat liver, and have a similar phenotype to that of early passage primary HSCs. CFSC cells are cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin. All cells are cultured in 6-well culture plates under 37°C and 5% CO2 in an incubator. The medium is replaced every two days, and the cells are harvested and diluted at a ratio of 1:3 twice a week. In experiments, HSCs are pretreated with the experimental concentration of Oleoylethanolamide (30 μM, 10 μM, 3 μM) before stimulation with 5 ng/mL TGF-β1. mRNA expression levels of α-SMA (A) and Col1a (B) are analyzed by real-time PCR[1]. |
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Animal experiment: |
Mice[1]The Sv/129 mice and PPAR-α knockout mice are maintained in a room with controlled temperature (21-23°C), humidity (55-60%) and lighting (12 h light/dark cycles) and given water ad libitum. Mice are randomly divided for methionine choline-deficient (MCD) and thioacetamide (TAA) experiments. In the MCD-diet feeding experiment, wild-type Sv/129 mice and PPAR-α knockout mice are each divided into three groups (n=8 /group): (i) control group receive normal diet; (ii) fed with MCD diet and injected with the vehicle (5% Tween-80+5% PEG400+90% saline, 5 mL/kg/day, 8 weeks, intraperitoneal injection, i.p.); (iii) fed with MCD diet along with Oleoylethanolamide administration (5 mg/kg/day; 8 weeks, i.p.). In another set of experiment, all the wild-type mice and PPAR-α knockout mice are given standard chow diet, and are randomly separated into three groups: the control group is not administrated TAA or Oleoylethanolamide but is injected with the saline; the TAA group is injected with TAA (160 mg/kg, three times per week, 6 weeks, dissolved in saline, i.p.) plus the corresponding vehicle; the Oleoylethanolamide group is both injected with TAA and Oleoylethanolamide (5 mg/kg/day; 6 weeks, i.p.)[1]. |
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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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| Cas No. | 111-58-0 | SDF | |
| Synonymes | Oleic Acid Ethanolamide, OEA | ||
| Chemical Name | (E)-N-(2-hydroxyethyl)octadec-9-enamide | ||
| Canonical SMILES | O=C(CCCCCCC/C=C/CCCCCCCC)NCCO | ||
| Formula | C20H39NO2 | M.Wt | 325.53 |
| Solubility | basic PBS: <100 µ g/ml,DMF: >100 mg/ml,DMSO: >100 mg/ml,EtOH: >100 mg/ml,PBS pH 7.2: <100 µ g/ml | Storage | Store at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.0719 mL | 15.3596 mL | 30.7191 mL |
| 5 mM | 0.6144 mL | 3.0719 mL | 6.1438 mL |
| 10 mM | 0.3072 mL | 1.536 mL | 3.0719 mL |
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- Purity: >90.00%
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