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Glycerophospho-N-Palmitoyl Ethanolamine Sale

(Synonyms: GPNAE, GPNPEA) 目录号 : GC40408

Precursor for palmitoyl ethanolamide

Glycerophospho-N-Palmitoyl Ethanolamine Chemical Structure

Cas No.:100575-09-5

规格 价格 库存 购买数量
1mg
¥1,147.00
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5mg
¥5,174.00
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10mg
¥9,181.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

N-Acylated ethanolamines (NAE) are naturally-occurring lipids that have diverse bioactivities. For example, arachidonoyl ethanolamide (AEA) is an endogenous neurotransmitter that evokes cellular responses by activating the cannabinoid receptors, central cannabinoid (CB1) and peripheral cannabinoid (CB2). The different types of NAE are derived from glycerophospho-linked precursors by the activity of glycerophosphodiesterase 1 (GDE1). Glycerophospho-N-palmitoyl ethanolamine (GP-NPEA) is the metabolic precursor of palmitoyl ethanolamide (PEA). PEA is an endogenous cannabinoid found in brain, liver, and other mammalian tissues, that has potent anti-inflammatory activity in vivo. PEA has low affinity for peripheral cannabinoid (CB2) and no appreciable affinity for central cannabinoid (CB1), suggesting that its efficacy is through a different receptor.

Chemical Properties

Cas No. 100575-09-5 SDF
别名 GPNAE, GPNPEA
Canonical SMILES CCCCCCCCCCCCCCCC(=O)NCCOP(=O)(O)OCC(O)CO
分子式 C21H44NO7P 分子量 453.6
溶解度 PBS (pH 7.2): 5 mg/ml 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.2046 mL 11.0229 mL 22.0459 mL
5 mM 0.4409 mL 2.2046 mL 4.4092 mL
10 mM 0.2205 mL 1.1023 mL 2.2046 mL
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Research Update

Quercetin improves high-fat diet-induced obesity by modulating gut microbiota and metabolites in C57BL/6J mice

Phytother Res 2022 Dec;36(12):4558-4572.PMID:35906097DOI:10.1002/ptr.7575.

High-fat diet-induced obesity is characterized by low-grade inflammation, which has been linked to gut microbiota dysbiosis. We hypothesized that quercetin supplementation would alter gut microbiota and reduce inflammation in obese mice. Male C57BL/6J mice, 4 weeks of age, were divided into 3 groups, including a low-fat diet group, a high-fat diet (HFD) group, and a high-fat diet plus quercetin (HFD+Q) group. The mice in HFD+Q group were given 50 mg per kg BW quercetin by gavage for 20 weeks. The body weight, fat accumulation, gut barrier function, glucose tolerance, and adipose tissue inflammation were determined in mice. 16 s rRNA amplicon sequence and non-targeted metabolomics analysis were used to explore the alteration of gut microbiota and metabolites. We found that quercetin significantly alleviated HFD-induced obesity, improved glucose tolerance, recovered gut barrier function, and reduced adipose tissue inflammation. Moreover, quercetin ameliorated HFD-induced gut microbiota disorder by regulating the abundance of gut microbiota, such as Adlercreutzia, Allobaculum, Coprococcus_1, Lactococcus, and Akkermansia. Quercetin influenced the production of metabolites that were linked to alterations in obesity-related inflammation and oxidative stress, such as Glycerophospho-N-Palmitoyl Ethanolamine, sanguisorbic acid dilactone, O-Phospho-L-serine, and P-benzoquinone. Our results demonstrate that the anti-obesity effects of quercetin may be mediated through regulation in gut microbiota and metabolites.

Metabolomics Analysis of the Prefrontal Cortex in a Rat Chronic Unpredictable Mild Stress Model of Depression

Front Psychiatry 2022 Mar 15;13:815211.PMID:35370823DOI:10.3389/fpsyt.2022.815211.

Background: Depressive disorder is the leading cause of disability and suicidality worldwide. Metabolites are considered indicators and regulators of depression. However, the pathophysiology of the prefrontal cortex (PFC) in depression remains unclear. Methods: A chronic unpredictable mild stress (CUMS) model and a maturation rodent model of depression was used to investigate metabolic changes in the PFC. Eighteen male Sprague-Dawley rats were randomly divided into CUMS and control groups. The sucrose preference test (SPT) and forced swimming test (FST) were employed to evaluate and record depression-associated behaviors and changes in body weight (BW). High-performance liquid chromatography-tandem mass spectrometry was applied to test metabolites in rat PFC. Furthermore, principal component analysis and orthogonal partial least-squares discriminant analysis were employed to identify differentially abundant metabolites. Metabolic pathways were analyzed using MetaboAnalyst. Finally, a metabolite-protein interaction network was established to illustrate the function of differential metabolites. Results: SPT and FST results confirmed successful establishment of the CUMS-induced depression-like behavior model in rats. Five metabolites, including 1-methylnicotinamide, 3-methylhistidine, acetylcholine, Glycerophospho-N-Palmitoyl Ethanolamine, α-D-mannose 1-phosphate, were identified as potential biomarkers of depression. Four pathways changed in the CUMS group. Metabolite-protein interaction analysis revealed that 10 pathways play roles in the metabolism of depression. Conclusion: Five potential biomarkers were identified in the PFC and metabolite-protein interactions associated with metabolic pathophysiological processes were explored using the CUMS model. The results of this study will assist physicians and scientists in discovering potential diagnostic markers and novel therapeutic targets for depression.