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1-Linoleoyl Glycerol Sale

(Synonyms: 一亚油酸甘油酯,1-Linoleoyl-rac-glycerol; 1-Monolinolein) 目录号 : GC35065

A PAF-AH inhibitor

1-Linoleoyl Glycerol Chemical Structure

Cas No.:2277-28-3

规格 价格 库存
10mM (in 1mL DMSO)
¥891.00
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100mg
¥810.00
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500mg
¥1,620.00
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产品描述

Platelet-activating factor (PAF) is a biologically active phospholipid synthesized by a variety of stimulated cells that acts as a mediator of platelet aggregation, inflammation, and allergy.1,2 PAF is converted to the biologically inactive lyso-PAF by the enzyme PAF acetylhydrolase (PAF-AH). Recently, plasma PAF-AH has been linked to atherosclerosis and may be a positive risk factor for coronary heart disease in humans.3 1-Linoleoyl glycerol (1-LG) is a fatty acid glycerol that has been isolated from S. chinensis roots. It inhibits PAF-AH with an IC50 of 45 ?M.4 1-LG has potential application in cholesterol lowering and antiatherogenic activity.

1.Prescott, S.M., Zimmerman, G.A., and McIntyre, T.M.Platelet-activating factorJ. Biol. Chem.265(29)17381-17384(1990) 2.Snyder, F.Platelet-activating factor and related acetylated lipids as potent biologically active cellular mediatorsAm. J. Physiol. Cell Physiol.259(5 Pt 1)C697-C708(1990) 3.Caslake, M.J., and Packard, C.J.Lipoprotein-associated phospholipase A2 (platelet-activating factor acetylhydrolase) and cardiovascular diseaseCurr. Opin. Lipidol.14347-352(2003) 4.Lee, W.S., Kim, M.J., Beck, Y.I., et al.Lp-PLA2 inhibitory activities of fatty acid glycerols isolated from Saururus chinensis rootsBioorg. Med. Chem. Lett.153573-3575(2005)

Chemical Properties

Cas No. 2277-28-3 SDF
别名 一亚油酸甘油酯,1-Linoleoyl-rac-glycerol; 1-Monolinolein
Canonical SMILES CCCCC/C=C\C/C=C\CCCCCCCC(OCC(O)CO)=O
分子式 C21H38O4 分子量 354.52
溶解度 DMSO: ≥ 100 mg/mL (282.07 mM); Ethanol: 100 mg/mL (282.07 mM) 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.8207 mL 14.1036 mL 28.2072 mL
5 mM 0.5641 mL 2.8207 mL 5.6414 mL
10 mM 0.2821 mL 1.4104 mL 2.8207 mL
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Research Update

Study on plasma metabolomics for HIV/AIDS patients treated by HAART based on LC/MS-MS

Front Pharmacol 2022 Aug 29;13:885386.PMID:36105186DOI:10.3389/fphar.2022.885386.

Background: Metabolomics can be applied to the clinical diagnosis and treatment evaluation of acquired immune deficiency syndrome (AIDS). AIDS biomarkers have become a new direction of AIDS research providing clinical guidance for diagnosis. Objective: We sought to apply both untargeted and targeted metabolomic profiling to identify potential biomarkers for AIDS patients. Methods: A liquid chromatography-tandem mass spectrometry (LC-MS/MS) based untargeted metabolomic profiling was performed on plasma samples of patients before and after highly active antiretroviral therapy (HAART) treatment as well as healthy volunteers to identify potential AIDS biomarkers. Targeted quantitative analysis was performed on the potential biomarkers screened from untargeted metabolic profiling for verification. Results: Using the Mass Profiler Professional and the MassHunter, several potential biomarkers have been found by LC-MS/MS in the untargeted metabolomic study. High-resolution MS and MS/MS were used to analyze fragmentation rules of the metabolites, with comparisons of related standards. Several potential biomarkers have been identified, including PS(O-18:0/0:0), sphingosine, PE (21:0/0:0), and 1-Linoleoyl Glycerol. Targeted quantitative analysis showed that sphingosine and 1-Linoleoyl Glycerol might be closely related to HIV/AIDS, which may be the potential biomarkers to the diagnosis. Conclusion: We conducted untargeted metabolomic profiling, which indicates that several metabolites should be considered potential biomarkers for AIDS patients. Further targeted metabolomic research verified that d-Sphingosine and 1-Linoleoyl Glycerol as the diagnostic biomarker of AIDS.

Hyperthermia-Induced Seizures Enhance Brain Concentrations of the Endocannabinoid-Related Linoleoyl Glycerols in a Scn1a+/- Mouse Model of Dravet Syndrome

Cannabis Cannabinoid Res 2022 Oct 21.PMID:36269656DOI:10.1089/can.2022.0145.

Introduction: The endocannabinoid system contributes to the homeostatic response to seizure activity in epilepsy, a disease of brain hyperexcitability. Indeed, studies using conventional epilepsy models have shown that seizures increase endocannabinoids in the brain. However, it is unknown whether endocannabinoids and structurally related fatty acid amides and monoacylglycerols are similarly released in response to acute seizures in animal models of drug-resistant epilepsy. Therefore, in this study, we investigated whether a hyperthermia-induced seizure increased concentrations of endocannabinoids and related signaling lipids in the Scn1a+/- mouse model of Dravet syndrome. Materials and Methods: We compared hippocampal concentrations of the major endocannabinoids and related monoglycerols and N-acylethanolamines in wild-type mice, naïve Scn1a+/- mice, and Scn1a+/- mice primed with a single, hyperthermia-induced, generalized tonic-clonic seizure. Samples were collected 5 and 60 min following the seizure and then analyzed with LC-MS/MS. Results: We found that a hyperthermia-induced seizure in Scn1a+/- mice did not affect hippocampal concentrations of the major endocannabinoids, 2-AG and anandamide, or the N-acylethanolamines studied, although the sampling of tissue 5 min postseizure may have been too late to capture any effect on these lipids. Heterozygous deletion of Scn1a alone did not affect these lipid signaling molecules. Notably, however, we found that a hyperthermia-induced seizure significantly increased hippocampal concentrations of the monoacylglycerols, 2-linoleoyl glycerol (2-LG) and 1-Linoleoyl Glycerol (1-LG), in Scn1a+/- mice. Conclusions: Our results show the unprecedented elevation of the lesser-studied endocannabinoid-related monoacylglycerols, 2-LG and 1-LG, following a hyperthermia-induced seizure in a mouse model of Dravet syndrome. Future research is needed to comprehensively explore the function of these lipid signaling molecules during seizure activity and whether their actions can be exploited to develop new therapeutics.

Molecularization of Bitter Off-Taste Compounds in Pea-Protein Isolates ( Pisum sativum L.)

J Agric Food Chem 2020 Sep 23;68(38):10374-10387.PMID:31896259DOI:10.1021/acs.jafc.9b06663.

Activity-guided fractionations, combined with taste dilution analyses (TDA), were performed to locate the key compounds contributing to the bitter off-taste of pea-protein isolates (Pisum sativum L.). Purification of the compounds perceived with the highest sensory impact, followed by 1D/2D-NMR, (LC-)MS/MS, LC-TOF-MS, and MSE experiments, led to the identification of 14 lipids and lipid oxidation products, namely, 9,10,13-trihydroxyoctadec-12-enoic acid, 9,12,13-trihydroxyoctadec-10-enoic acid, 9,10,11-trihydroxyoctadec-12-enoic, 11,12,13-trihydroxyoctadec-9-enoic acid, (10E,12E)-9-hydroxyoctadeca-10,12-dienoic acid, (9Z,11E)-13-hydroxyoctadeca-9,11-dienoic acid, (9E,11E)-13-hydroxyoctadeca-9,11-dienoic acid, 1-Linoleoyl Glycerol, α-linolenic acid, 2-hydroxypalmitic acid, 2-hydroxyoleic acid, linoleic acid, (9Z,11E)-13-oxooctadeca-9,11-dienoic acid, and octacosa-6,9,19,22-tetraen. Herein, we present the isolation, structure determination, and sensory activity of these molecules. Depending on their structure, the isolated compounds showed human bitter recognition thresholds between 0.06 and 0.99 mmol/L in water.

Apolipoprotein CIII regulates lipoprotein-associated phospholipase A2 expression via the MAPK and NFκB pathways

Biol Open 2015 Apr 2;4(5):661-5.PMID:25836672DOI:10.1242/bio.201410900.

Apolipoprotein CIII (apo CIII), a small glycoprotein that binds to the surfaces of certain lipoproteins, is associated with inflammatory and atherogenic responses in vascular cells. Lipoprotein-associated phospholipase A2 (Lp-PLA2) has been proposed as an inflammatory biomarker and potential therapeutic target for cardiovascular disease (CVD). Here, we report that apo CIII increases Lp-PLA2 mRNA and protein levels in dose- and time- dependent manner in human monocytic THP-1 cells, and the increase can be abolished by MAPK and NFκB pathway inhibitors. Lp-PLA2 inhibitor, 1-Linoleoyl Glycerol attenuates the inflammation induced by apo CIII. In turn, exogenous Lp-PLA2 expression upregulates apo CIII and the upregulation can be inhibited by 1-Linoleoyl Glycerol in HepG2 cells. Moreover, plasma Lp-PLA2 level is correlated with apo CIII expression in pig liver. In vivo, Lp-PLA2 expression in monocytes and its activity in serum were significantly increased in human apo CIII transgenic porcine models compared with wild-type pigs. Our results suggest that Lp-PLA2 and apo CIII expression level is correlated with each other in vitro and in vivo.

Quantification and Bitter Taste Contribution of Lipids and Their Oxidation Products in Pea-Protein Isolates ( Pisum sativum L.)

J Agric Food Chem 2021 Aug 11;69(31):8768-8776.PMID:34324814DOI:10.1021/acs.jafc.1c02889.

An ultra-high-performance liquid chromatography-differential ion mobility (DMS)-tandem mass spectrometry method was developed to quantify 14 bitter-tasting lipids in 17 commercial pea-protein isolates (Pisum sativum L.). The DMS technology enabled the simultaneous quantification of four hydroxyoctadecadienoic acid isomers, namely, (10E,12Z)-9-hydroxyoctadeca-10,12-dienoic acid (5), (10E,12E)-9-hydroxyoctadeca-10,12-dienoic acid (6), (9Z,11E)-13-hydroxyoctadeca-9,11-dienoic acid (7), and (9E,11E)-13-hydroxyoctadeca-9,11-dienoic acid (8). Based on quantitative data and human bitter taste recognition thresholds, dose-over-threshold factors were determined to evaluate the individual lipids' bitter impact and compound classes. The free fatty acids α-linolenic acid (10) and linoleic acid (13), as well as the trihydroxyoctadecenoic acids, especially 9,10,11-trihydroxyoctadec-12-enoic (3), and 11,12,13-trihydroxyoctadec-9-enoic acids (4), were shown to be key inducers to bitterness in the isolates. Additionally, the impact of 1-Linoleoyl Glycerol (9) on the bitter taste could be shown for 14 of the 17 tested pea-protein isolates.