tetranor-PGEM
(Synonyms: tetranor-Prostaglandin E Metabolite) 目录号 : GC45026A metabolite of PGE2
Cas No.:24769-56-0
Sample solution is provided at 25 µL, 10mM.
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tetranor-PGEM is the major urinary metabolite of PGE1 and PGE2, and is used as a marker of PGE2 biosynthesis.[1],[2] About 15% of an infused dose of PGE2 appears as this metabolite in the urine of humans. Normal healthy males excrete 7-40 µg of tetranor-PGEM over a 24-hour period.[1]
Reference:
[1]. Hamberg, M. Inhibition of prostaglandin synthesis in man. Biochemical and Biophysical Research Communications 49, 720-726 (1972).
[2]. Honda, H., Fukawa, K., and Sawabe, T. Influence of adjuvant arthritis on main urinary metabolites of prostaglandin F and E rats. Prostaglandins 19, 259-269 (1980).
Cas No. | 24769-56-0 | SDF | |
别名 | tetranor-Prostaglandin E Metabolite | ||
化学名 | 9,15-dioxo-11α-hydroxy-13,14-dihydro-2,3,4,5-tetranor-prostan-1,20-dioic acid | ||
Canonical SMILES | O[C@H]1[C@H](CCC(CCCCC(O)=O)=O)[C@@H](CCC(O)=O)C(C1)=O | ||
分子式 | C16H24O7 | 分子量 | 328.4 |
溶解度 | 50mg/mL in DMSO, or in DMF | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 3.0451 mL | 15.2253 mL | 30.4507 mL |
5 mM | 0.609 mL | 3.0451 mL | 6.0901 mL |
10 mM | 0.3045 mL | 1.5225 mL | 3.0451 mL |
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给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
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2.
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Development of Monoclonal Antibody-Based EIA for Tetranor-PGDM which Reflects PGD2 Production in the Body
J Immunol Res 2021 Apr 26;2021:5591115.PMID:33997056DOI:10.1155/2021/5591115.
Tetranor-PGDM is a metabolite of PGD2. Urinary tetranor-PGDM levels were reported to be increased in some diseases, including food allergy, Duchenne muscular dystrophy, and aspirin-intolerant asthma. In this study, we developed a monoclonal antibody (MAb) and a competitive enzyme immunoassay (EIA) for measuring tetranor-PGDM. Spleen cells isolated from mice immunized with tetranor-PGDM were utilized to generate Ab-producing hybridomas. We chose hybridomas and purified MAb against tetranor-PGDM to develop competitive EIA. The assay evaluated the optimal ionic strength, pH, precision, and reliability. Specificity was determined by cross-reactivity to tetranor-PGEM, tetranor-PGFM, and tetranor-PGAM. Recovery was determined by spiking experiments on artificial urine. Optimal ionic strength was 150 mM NaCl, and optimal pH was pH 7.5. Metabolites other than tetranor-PGDM did not show any significant cross-reactivity in the EIA. The assay exhibited a half-maximal inhibition concentration (IC50) of 1.79 ng/mL, limit of detection (LOD) of 0.0498 ng/mL, and range of quantitation (ROQ) value of 0.252 to 20.2 ng/mL. The intra- and inter-assay variation for tetranor-PGDM was 3.9-6.0% and 5.7-10.4%, respectively. The linearity-dilution effect showed excellent linearity under dilution when artificial urine samples were applied to solid-phase extraction (SPE). After SPE, recovery of tetranor-PGDM in artificial urine averaged from 82.3% to 113.5% and was within acceptable limits (80%-120%). We successfully generated one monoclonal antibody and developed a sensitive competitive EIA. The established EIA would be useful for routine detection and monitoring of tetranor-PGDM in research or diagnostic body fluids.
Simultaneous analyses of urinary eicosanoids and related mediators identified tetranor-prostaglandin E metabolite as a novel biomarker of diabetic nephropathy
J Lipid Res 2021;62:100120.PMID:34560080DOI:10.1016/j.jlr.2021.100120.
Diabetic nephropathy is a major complication of diabetes mellitus, and thus novel biomarkers are desired to evaluate the presence and progression of diabetic nephropathy. In this study, we sought to identify possible metabolites related to diabetic nephropathy among urinary eicosanoids and related mediators. Using liquid chromatogram-tandem mass spectrometry, we optimized the lipid extraction from urine using the Monospin C18 as a solid-phase extraction cartridge and measured the urinary lipid mediators in 111 subjects with type 2 diabetes mellitus as well as 33 healthy subjects. We observed that 14 metabolites differed significantly among the clinical stages of nephropathy. Among them, levels of tetranor-prostaglandin E metabolite (tetranor-PGEM), an arachidonic acid metabolite, were significantly higher in subjects with stage 1 nephropathy than in healthy subjects and increased with the progression of nephropathy. We also observed that levels of maresin-1, a docosahexaenoic acid metabolite, and leukotriene B4-ethanolamide, an arachidonoyl ethanolamide metabolite, were significantly lower in subjects with stage 3-4 nephropathy than in healthy subjects and those with stage 1-2 nephropathy. Finally, using a comprehensive analysis of urinary eicosanoids and related mediators, we concluded that tetranor-PGEM was capable of discriminating clinical stages of nephropathy and thus useful as a novel biomarker for diabetic nephropathy.
Evaluation of urinary prostaglandin E2 metabolite as a biomarker in infants with fever due to viral infection
Prostaglandins Leukot Essent Fatty Acids 2014 Dec;91(6):269-75.PMID:25305792DOI:10.1016/j.plefa.2014.09.006.
We have investigated the clinical feasibility of the major urinary metabolite of prostaglandin (PG) E2, tetranor-PGEM, as a biomarker of inflammation in infants with fever. We tested two different and clinically relevant sampling methods, using self-adhesive urinary bags or gauze pads, with respect to stability of tetranor-PGEM and ease of sampling from infants. Liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis was used to quantify tetranor-PGEM in urine, and different normalization parameters, i.e., urinary creatinine and body surface area, were investigated. To study inflammation, infants (1 month-1 year) that were hospitalized with fever of unknown origin at admittance (n=14) were compared to age-matched healthy controls (n=14). Levels of urinary tetranor-PGEM in infants with viral induced fever were increased compared to controls (102.4±56.2 vs. 37.0±21.6pmol/ml/m(2) body surface area, p<0.001). We conclude that urinary tetranor-PGEM is a potential non-invasive biomarker of inflammation in infants.
Modulations of urinary lipid mediators in acute bladder cystitis
Prostaglandins Other Lipid Mediat 2023 Feb;164:106690.PMID:36332874DOI:10.1016/j.prostaglandins.2022.106690.
Bioactive lipids, such as lysophospholipids, ceramides, and eicosanoids and related mediators, have been demonstrated to be involved in inflammation. We aimed to investigate the possible orchestral modulations of these bioactive lipids in human inflammation. We simultaneously measured the urinary levels of lysophospholipids, ceramides, and eicosanoids and related mediators by a liquid chromatography-mass spectrometry method in patients with cystitis and control subjects. The urinary levels of lysophosphatidylcholine, lysophosphatidylethanolamine, sphingosine 1-phosphate, ceramides, prostaglandin (PG)E2 and its metabolites represented by tetranor-PGEM, several oxylipins, DHA, and lysoPAF were higher in patients with cystitis. Urinary levels of some species of glycerolysophospholipids were highly positively correlated with those of other species of the same glycerolysophospholipids. Cluster analyses revealed that lysophosphatidylcholine was close to a PGE2 metabolite, lysophosphatidylethanolamine was close to DHA, and sphingosine 1-phosphate and ceramides were close to lysoPAF. The orchestral dynamism of the lipid mediators was observed in the urine of cystitis, suggesting the necessity for simultaneous investigation of lipid mediators for translational research.
Urinary prostaglandin D2 and E2 metabolites associate with abdominal obesity, glucose metabolism, and triglycerides in obese subjects
Prostaglandins Other Lipid Mediat 2019 Dec;145:106361.PMID:31419481DOI:10.1016/j.prostaglandins.2019.106361.
Obesity is associated with low-grade chronic inflammation, which contributes to the development of the metabolic syndrome and its associated complications, such as insulin resistance and type-2 diabetes. Limited data from animal and human studies support local generation of pro-inflammatory prostanoid lipid mediators in white adipose tissue. However, the link between systemic prostanoid levels and parameters characterizing the metabolic syndrome is missing in human obesity. Therefore, we performed a targeted lipidomic analysis using urine samples from obese human subjects (n = 45) and show for the first time in humans that urinary prostanoid levels correlate with metabolic parameters that indicate a dysregulated glucose and triglyceride metabolism. We identified tetranor-PGDM and tetranor-PGEM as the two major urinary prostanoid metabolites in obese subjects with levels of 247 ± 31 and 23.3 ± 4.0 pmol/mg creatinine, respectively. Tetranor-PGDM was significantly associated with serum triglycerides, while tetranor-PGEM was associated with abdominal obesity as defined by an increased waist-to-hip ratio (WHR), with glycated hemoglobin (HbA1c), and with impaired oral glucose tolerance. These results confirm the previously established notion of low-grade chronic inflammation in obesity and further identify an association of the prostanoid pathway with obesity-associated dyslipidemia, abdominal obesity, and insulin resistance.