9-Nitrooleate
(Synonyms: 9-硝基油酸) 目录号 : GC42649A novel endogenous lipid signalling molecule
Cas No.:875685-44-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Nitrated unsaturated fatty acids, such as 10- and 12-nitrolinoleate , cholesteryl nitrolinoleate, and nitrohydroxylinoleate, represent a new class of endogenous lipid-derived signalling molecules. LNO2 isomers serve as potent endogenous ligands for PPARγ and can also decompose or be metabolized to release nitric oxide. 9-Nitrooleate is one of two regioisomers of nitrooleate, the other being 10-nitrooleate (OA-NO2; used for the mixture of isomers), which are formed by nitration of oleic acid in approximately equal proportions in vivo. Peroxynitrite, acidified nitrite, and myeloperoxidase in the presence of H2O2 and nitrite, all mediate the nitration of oleic acid. OA-NO2 is found in human plasma as the free acid and esterified in phospholipids at concentrations of 619 ± 52 nM and 302 ± 369 nM, respectively. OA-NO2 activates PPARγ approximately 7-fold at a concentration of 1 µM and effectively promotes differentiation 3T3-L1 preadipocytes to adipocytes at 3 µM.
| Cas No. | 875685-44-2 | SDF | |
| 别名 | 9-硝基油酸 | ||
| Canonical SMILES | CCCCCCCC/C=C([N+]([O-])=O)\CCCCCCCC(O)=O | ||
| 分子式 | C18H33NO4 | 分子量 | 327.5 |
| 溶解度 | Ethanol: 1 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 | 3.0534 mL | 15.2672 mL | 30.5344 mL |
| 5 mM | 0.6107 mL | 3.0534 mL | 6.1069 mL |
| 10 mM | 0.3053 mL | 1.5267 mL | 3.0534 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。
Surface Active Salivary Metabolites Indicate Oxidative Stress and Inflammation in Obstructive Sleep Apnea
Allergy Asthma Immunol Res 2023 May;15(3):316-335.PMID:37075797DOI:10.4168/aair.2023.15.3.316.
Purpose: Obstructive sleep apnea (OSA), a highly prevalent and potentially serious sleep disorder, requires effective screening tools. Saliva is a useful biological fluid with various metabolites that might also influence upper airway patency by affecting surface tension in the upper airway. However, little is known about the composition and role of salivary metabolites in OSA. Therefore, we investigated the metabolomics signature in saliva from the OSA patients and evaluated the associations between identified metabolites and salivary surface tension. Methods: We studied 68 subjects who visited sleep clinic due to the symptoms of OSA. All underwent full-night in-lab polysomnography. Patients with apnea-hypopnea index (AHI) < 10 were classified to the control, and those with AHI ≥ 10 were the OSA groups. Saliva samples were collected before and after sleep. The centrifuged saliva samples were analyzed by liquid chromatography with high-resolution mass spectrometry (ultra-performance liquid chromatography-tandem mass spectrometry; UPLC-MS/MS). Differentially expressed salivary metabolites were identified using open source software (XCMS) and Compound Discoverer 2.1. Metabolite set enrichment analysis (MSEA) was performed using MetaboAnalyst 5.0. The surface tension of the saliva samples was determined by the pendant drop method. Results: Three human-derived metabolites (1-palmitoyl-2-[5-hydroxyl-8-oxo-6-octenoyl]-sn-glycerol-3-phosphatidylcholine [PHOOA-PC], 1-palmitoyl-2-[5-keto-8-oxo-6-octenoyl]-sn-glycerol-3-phosphatidylcholine [KPOO-PC], and 9-Nitrooleate) were significantly upregulated in the after-sleep salivary samples from the OSA patients compared to the control group samples. Among the candidate metabolites, only PHOOA-PC was correlated with the AHI. In OSA samples, salivary surface tension decreased after sleep. The differences in surface tension were negatively correlated with PHOOA-PC and 9-Nitrooleate concentrations. Furthermore, MSEA revealed that arachidonic acid-related metabolism pathways were upregulated in the after-sleep samples from the OSA group. Conclusions: This study revealed that salivary PHOOA-PC was correlated positively with the AHI and negatively with salivary surface tension in the OSA group. Salivary metabolomic analysis may improve our understanding of upper airway dynamics and provide new insights into novel biomarkers and therapeutic targets in OSA.
Oral ibuprofen differentially affects plasma and sweat lipid mediator profiles in healthy adult males
Prostaglandins Other Lipid Mediat 2018 Jul;137:1-8.PMID:29778785DOI:10.1016/j.prostaglandins.2018.05.009.
Sweat contains a variety of lipid mediators, but whether they originate from the plasma filtrate or from the cutaneous sweat glandular tissues themselves is unknown. To explore this knowledge gap, we collected plasma and sweat from healthy men (n = 9) immediately before and 0.5, 2 and 4 h after oral administration of 400 mg ibuprofen. Of the over 100 lipid mediators assayed by liquid chromatography-tandem mass spectrometry, ∼45 were detected in both plasma and sweat, and 36 were common to both matrices. However, baseline concentrations in each matrix were not correlated and metabolite relative abundances between matrices differed. Oral ibuprofen administration altered sweat lipid mediators, reducing prostaglandin E2, linoleoylethanolamide, and oleoylethanolamide, while increasing 11-hydroxyeicosatetraenoic acid, and causing transient changes in 9-Nitrooleate, N-arachidonylglycine and 20-hydroxyeicosatetraenoic acid. Meanwhile, plasma N-acylethanolamide concentrations increased with ibuprofen administration. These results suggest that sweat and plasma differentially reflect biochemical changes due to oral ibuprofen administration, and that plasma is unlikely to be the predominant source of the sweat lipid mediator profile.