Lyso-PAF C-16
(Synonyms: 1-O-十六烷基-SN-甘油基-3-胆碱磷酸) 目录号 : GC44103A precursor of PAF
Cas No.:52691-62-0
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Lyso-PAF C-16 can be formed by either the action of PAF-AH on PAF C-16, or by the action of a CoA-independent transacylase on 1-O-hexadecyl-2-acyl-glycerophosphocholine. Lyso-PAF C-16 is a substrate for either PAF C-16 formation by the remodeling pathway or selective acylation with arachidonic acid by a CoA-independent transacylase.
Cas No. | 52691-62-0 | SDF | |
别名 | 1-O-十六烷基-SN-甘油基-3-胆碱磷酸 | ||
Canonical SMILES | CCCCCCCCCCCCCCCCOC[C@@H](O)COP(OCC[N+](C)(C)C)([O-])=O | ||
分子式 | C24H52NO6P | 分子量 | 481.7 |
溶解度 | DMF: 10 mg/ml,DMSO: 10 mg/ml,Ethanol: 10 mg/ml,PBS (pH 7.2): 10 mg/ml,Water: 20 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 | |||
1 mg | 5 mg | 10 mg | |
1 mM | 2.076 mL | 10.3799 mL | 20.7598 mL |
5 mM | 0.4152 mL | 2.076 mL | 4.152 mL |
10 mM | 0.2076 mL | 1.038 mL | 2.076 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。
Serum metabolomics analysis of mice that received repeated airway exposure to a water-soluble PM2.5 extract
Ecotoxicol Environ Saf 2019 Jan 30;168:102-109.PMID:30384157DOI:10.1016/j.ecoenv.2018.10.068.
Background: Air pollutant exposure negatively affects human health; however, the molecular mechanisms causing disease remain largely unclear. Objectives: To explore the effects of respiratory particulate matter (PM2.5) exposure on the serum metabolome and to identify biomarkers for risk assessment of PM2.5 exposure. Methods: PM2.5 from Nanjing, China, was collected, and its water-soluble extract was subjected to component analysis. BALB/c mice received acute or prolonged exposure to insoluble PM2.5 particles or its water-soluble extract, and lung tissue was submitted to histopathological analyses. Serum samples were collected pre- and post-PM2.5 exposure and analyzed by liquid chromatography/mass spectrometry. Results: Component analysis revealed that metals and inorganic ions were the most abundant components in the soluble PM2.5 samples. Acute exposure to insoluble PM2.5 particles and prolonged exposure to the water-soluble PM2.5 extract both induced severe lung injury, and the lung histopathological scores were significantly associated with PM2.5 exposure. Metabolomics analysis showed that prolonged exposure to the water-soluble PM2.5 extract was associated with statistically significant metabolite changes; the serum concentrations of 30 known metabolites, including metabolites of phospholipids, amino acids and sphingolipids, differed significantly between the control and PM2.5 exposure group. Pathway analysis identified an association of the tricarboxylic acid cycle (TCA) and the phospholipase metabolism pathway with PM2.5 exposure. The most influential metabolites for discriminating between the PM2.5-exposure group serum and the control serum were LysoPE, LysoPC, LGPC, citric acid, PAF C-18, NeuAcalpha2-3Galbeta-Cer, Lyso-PAF C-16, ganglioside GA2, 1-sn-glycero-3-phosphocholine, PC and L-tryptophan. Conclusions: Respiratory exposure to water-soluble PM2.5 extract has developmental consequences affecting not only the respiratory system but also metabolism.