20-HEPE
目录号 : GC40377
An EPA metabolite
Cas No.:116477-57-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
20-HEPE is a metabolite of eicosapentaenoic acid that is formed via ω-oxidation of EPA by cytochrome P450 (CYP) ω-oxidases, including human CYP4F3B. It activates peroxisome proliferator-activated receptor α (PPARα) in COS-7 cells expressing a luciferase reporter when used at a concentration of 10 μM. 20-HEPE also activates murine transient receptor potential vanilloid receptor 1 (mTRPV1) in vitro but lacks antinociceptive activity in rats.
| Cas No. | 116477-57-7 | SDF | |
| Canonical SMILES | OCC/C=C\C/C=C\C/C=C\C/C=C\C/C=C\CCCC(O)=O | ||
| 分子式 | C20H30O3 | 分子量 | 318.5 |
| 溶解度 | DMF: miscible,DMSO: miscible,Ethanol: miscible,PBS (pH 7.2): 0.8 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 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。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.1397 mL | 15.6986 mL | 31.3972 mL |
| 5 mM | 0.6279 mL | 3.1397 mL | 6.2794 mL |
| 10 mM | 0.314 mL | 1.5699 mL | 3.1397 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Chemical synthesis and biological evaluation of ω-hydroxy polyunsaturated fatty acids
Bioorg Med Chem Lett 2017 Feb 1;27(3):620-625.PMID:28025003DOI:10.1016/j.bmcl.2016.12.002.
ω-Hydroxy polyunsaturated fatty acids (PUFAs), natural metabolites from arachidonic acid (ARA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were prepared via convergent synthesis approach using two key steps: Cu-mediated CC bond formation to construct methylene skipped poly-ynes and a partial alkyne hydrogenation where the presence of excess 2-methyl-2-butene as an additive that is proven to be critical for the success of partial reduction of the poly-ynes to the corresponding cis-alkenes without over-hydrogenation. The potential biological function of ω-hydroxy PUFAs in pain was evaluated in naive rats. Following intraplantar injection, 20-hydroxyeicosatetraenoic acid (20-HETE, ω-hydroxy ARA) generated an acute decrease in paw withdrawal thresholds in a mechanical nociceptive assay indicating pain, but no change was observed from rats which received either 20-hydroxyeicosapentaenoic acid (20-HEPE, ω-hydroxy EPA) or 22-hydroxydocosahexaenoic acid (22-HDoHE, ω-hydroxy DHA). We also found that both 20-HEPE and 22-HDoHE are more potent than 20-HETE to activate murine transient receptor potential vanilloid receptor1 (mTRPV1).
Comprehensive Analysis of Fatty Acid and Oxylipin Patterns in n3-PUFA Supplements
J Agric Food Chem 2022 Apr 6;70(13):3979-3988.PMID:35324176DOI:10.1021/acs.jafc.1c07743.
Supplementing long-chain omega-3 polyunsaturated fatty acids (n3-PUFA) improves health. We characterized the pattern of total and non-esterified oxylipins and fatty acids in n3 supplements made of fish, krill, or micro-algae oil by LC-MS. All supplements contained the declared amount of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA); however, their content per capsule and the concentration of other fatty acids varied strongly. Krill oil contained the highest total n3 oxylipin concentration (6000 nmol/g) and the highest degree of oxidation (EPA 0.7%; DHA 1.3%), while micro-algae oil (Schizochytrium sp.) showed the lowest oxidation (<0.09%). These oils contain specifically high amounts of the terminal hydroxylation product of EPA (20-HEPE, 300 nmol/g) and DHA (22-HDHA, 200 nmol/g), which can serve as an authenticity marker for micro-algae oil. Refined micro-algae and fish oil were characterized by NEFA levels of ≤0.1%. Overall, the oxylipin and fatty acid pattern allows gaining new insights into the origin and quality of n3-PUFA oils in supplements.
Dexamethasone induces bisallylic hydroxylation of polyunsaturated fatty acids by rat liver microsomes
Arch Biochem Biophys 1996 Aug 15;332(2):261-8.PMID:8806734DOI:10.1006/abbi.1996.0341.
Human, monkey, and rat liver microsomes catalyze bisallylic hydroxylations of arachidonic and linoleic acids. The cytochrome P450 gene family of these hydroxylases has not been determined. We examined whether inducers of cytochrome P450 could augment the bisallylic hydroxylation activity of male rat liver microsomes. The microsomes were incubated with [14C]linoleic acid and NADPH and the monohydroxy metabolites were characterized. Microsomes prepared from control rats yielded mainly 18-hydroxyoctadecadienoic acid (18-HODE) and 17-HODE and microsomes from clofibrate-treated rats 18-HODE. Microsomes from beta-naphthoflavone-treated rats hydroxylated linoleic acid without position specificity, i.e., at carbons 8, 11, 14, 16, 17, and 18. 11-HODE, 17-HODE, and 18-HODE were major metabolites. Microsomes from rats treated with phenobarbital, isopropanol, imidazole, or acetone also formed these three products along with many other hydroxy metabolites. The synthetic glucocorticoid dexamethasone increased the biosynthesis of 11-HODE selectively. Microsomes from male Sprague-Dawley and Fischer rats treated with dexamethasone mainly formed 11-HODE and 18-HODE. The biosynthesis of 11-HODE was increased 10-fold and troleandomycin (50 microM) inhibited the biosynthesis of 11-HODE by 90%. The bisallylic hydroxylases were also investigated with 14C-labeled arachidonic and eicosapentaenoic acids as substrates. Microsomes from rats treated with dexamethasone converted 20:4n-6 to 13-hydroxyeicosatetraenoic acid (13-HETE), 10-HETE, 7-HETE, 19-HETE, and 20-HETE. Induction by acetone yielded the same products. Microsomes from dexamethasone-treated rats metabolized 20:5n-3 to 16-hydroxyeicosapentaenoic acid (16-HEPE), 13-HEPE, 10-HEPE, 19-HEPE, and 20-HEPE as major products, while microsomes from control and acetone-treated rats mainly formed 19-HEPE and 20-HEPE. We conclude that microsomes from dexamethasone-treated rats catalyze bisallylic hydroxylations of 18:2n-6, 20:4n-6, and 20:5n-3, possibly by induction of bisallylic hydroxylases of the CYP3A subfamily.
APOE Genotype Modifies the Plasma Oxylipin Response to Omega-3 Polyunsaturated Fatty Acid Supplementation in Healthy Individuals
Front Nutr 2021 Sep 17;8:723813.PMID:34604280DOI:10.3389/fnut.2021.723813.
The omega-3 polyunsaturated fatty acids (n-3 PUFAs), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), mediate inflammation in large part by affecting pro-inflammatory and anti-inflammatory/pro-resolving oxylipin concentrations. Common gene variants are thought to underlie the large inter-individual variation in oxylipin levels in response to n-3 PUFA supplementation, which in turn is likely to contribute to the overall heterogeneity in response to n-3 PUFA intervention. Given its known role in inflammation and as a modulator of the physiological response to EPA and DHA, here we explore, for the first time, the differential response of plasma hydroxy-, epoxy- and dihydroxy-arachidonic acid, EPA and DHA oxylipins according to apolipoprotein E (APOE) genotype using samples from a dose-response parallel design RCT. Healthy participants were given doses of EPA+DHA equivalent to intakes of 1, 2, and 4 portions of oily fish per week for 12 months. There was no difference in the plasma levels of EPA, DHA or ARA between the wildtype APOE3/E3 and APOE4 carrier groups after 3 or 12 months of n-3 PUFA supplementation. At 12 months, hydroxy EPAs (HEPEs) and hydroxy-DHAs (HDHAs) were higher in APOE4 carriers, with the difference most evident at the highest EPA+DHA intake. A significant APOE*n-3 PUFA dose effect was observed for the CYP-ω hydroxylase products 19-HEPE (p = 0.027) and 20-HEPE (p = 0.011). 8-HEPE, which, along with several other plasma oxylipins, is an activator of peroxisome proliferator activated receptors (PPARs), showed the highest fold change in APOE4 carriers (14-fold) compared to APOE3/E3 (4-fold) (p = 0.014). Low basal plasma EPA levels (EPA < 0.85% of total fatty acids) were associated with a greater change in 5-HEPE, 9-HEPE, 11-HEPE, and 20-HEPE compared to high basal EPA levels (EPA > 1.22% of total fatty acids). In conclusion, APOE genotype modulated the plasma oxylipin response to increased EPA+DHA intake, with APOE4 carriers presenting with the greatest increases following high dose n-3 PUFA supplementation for 12 months.
The PNPLA3 variant I148M reveals protective effects toward hepatocellular carcinoma in mice via restoration of omega-3 polyunsaturated fats
J Nutr Biochem 2022 Oct;108:109081.PMID:35691594DOI:10.1016/j.jnutbio.2022.109081.
Alcohol consumption and high caloric diet are leading causes of progressive fatty liver disease. Genetic variant rs738409 in patatin-like phospholipase domain-containing protein 3 (PNPLA3 rs738409 C>G) has been repeatedly described as one of the major risk loci for alcoholic liver cirrhosis (ALC) and hepatocellular carcinoma (HCC) in humans, however, the mechanism behind this association is incompletely understood. We generated mice carrying the rs738409 variant (PNPLA3 I148M) in order to detect genotype-phenotype relationships in mice upon chow and alcohol-high fat/high sugar diet (EtOH/WD). We could clearly demonstrate that the presence of rs738409 per se is sufficient to induce spontaneous development of steatosis after 1 year in mice on a chow diet, whereas in the setting of unhealthy diet feeding, PNPLA3 I148M did not affect hepatic inflammation or fibrosis, but induced a striking lipid remodeling, microvesicular steatosis and protected from HCC formation. Using shot gun lipidomics, we detected a striking restoration of reduced long chain-polyunsaturated fatty acids (LC-PUFA)-containing TGs, docosapentaenoic acid (C22:5 n3) and omega-3-derived eicosanoids (5-HEPE, 20-HEPE, 19,20-EDP, 21-HDHA) in PNPLA3 I148M mice upon EtOH/WD. At the molecular level, PNPLA3 I148M modulated enzymes for fatty acid and TG transport and metabolism. These findings suggest (dietary) lipids as an important and independent driver of hepatic tumorigenesis. Genetic variant in PNPLA3 exerted protective effects in mice, conflicting with findings in humans. Species-related differences in physiology and metabolism should be taken into account when modeling unhealthy human lifestyle, as genetic mouse models may not always allow for translation of insight gained in humans.