1-Salicylate Glucuronide
(Synonyms: Salicyl Phenolic Glucuronide, Salicylic Acid Phenolic Glucuronide) 目录号 : GC49366A metabolite of salicylic acid and aspirin
Cas No.:7695-70-7
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
1-Salicylate glucuronide is a metabolite of salicylic acid and aspirin .1 It is formed from salicylic acid primarily by the UDP-glucuronosyltransferase (UGT) isoform UGT1A9 but also by a variety of other UGT isoforms and from aspirin via salicylic acid as an intermediate.
1.Kuehl, G.E., Bigler, J., Potter, J.D., et al.Glucuronidation of the aspirin metabolite salicylic acid by expressed UDP-glucuronosyltransferases and human liver microsomesDrug Metab. Dispos.34(2)199-202(2006)
| Cas No. | 7695-70-7 | SDF | |
| 别名 | Salicyl Phenolic Glucuronide, Salicylic Acid Phenolic Glucuronide | ||
| Canonical SMILES | OC([C@H]([C@H]([C@@H]([C@H]1O)O)O)O[C@H]1OC2=C(C=CC=C2)C(O)=O)=O | ||
| 分子式 | C13H14O9 | 分子量 | 314.2 |
| 溶解度 | Methanol: slightly soluble,Water: slightly soluble | 储存条件 | -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 | 3.1827 mL | 15.9134 mL | 31.8269 mL |
| 5 mM | 0.6365 mL | 3.1827 mL | 6.3654 mL |
| 10 mM | 0.3183 mL | 1.5913 mL | 3.1827 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。
Metabolomics analysis of urine from rats administered with long-term, low-dose acrylamide by ultra-performance liquid chromatography-mass spectrometry
Xenobiotica 2017 May;47(5):439-449.PMID:27347750DOI:10.1080/00498254.2016.1196509.
1. To study the toxic effect of chronic exposure to acrylamide (AA) at low-dose levels, we applied metabolomics approach based on ultra-performance liquid chromatography/mass spectrometry (UPLC-MS). A total of 40 male Wistar rats were randomly assigned to different groups: control, low-dose AA (0.2 mg/kg.bw), middle-dose AA (1 mg/kg.bw) and high-dose AA (5 mg/kg.bw). The rats continuously received AA via drinking water for 16 weeks. Rat urine samples were collected at different time points for measurement of metabolomic profiles. 2. Thirteen metabolites, including the biomarkers of AA exposure (AAMA, GAMA and iso-GAMA), were identified from the metabolomic profiles of rat urine. Compared with the control group, the treated groups showed significantly increased intensities of GAMA, AAMA, iso-GAMA, vinylacetylglycine, 1-Salicylate Glucuronide, PE (20:1(11Z)/14:0), cysteic acid, L-cysteine, p-cresol sulfate and 7-ketodeoxycholic acid, as well as decreased intensities of 3-acetamidobutanal, 2-indolecarboxylic acid and kynurenic acid in rat urine. Notably, three new candidate biomarkers (p-cresol sulfate, 7-ketodeoxycholic acid and 1-Salicylate Glucuronide) in rat urine exposed to AA have been found in this study. 3. The results indicate exposure to AA disrupts the metabolism of lipids and amino acids, induces oxidative stress.
Metabonomic analysis of quercetin against the toxicity of acrylamide in rat urine
Food Funct 2017 Mar 22;8(3):1204-1214.PMID:28224155DOI:10.1039/c6fo01553k.
This research aims to determine whether quercetin has protective effects against the toxicity of acrylamide (AA) using metabonomic technology. Randomly, the rats were assigned into a control group, AA treatment group, quercetin treatment group and quercetin plus AA treatment group. Quercetin and AA were administered to rats daily via gavage and drinking water for 16 weeks, respectively. To detect the metabonomic profiles of urine, ultra-performance liquid chromatography/mass spectrometry was used. A total of 15 metabolites, including biomarkers of AA exposure (GAMA, AAMA, and iso-AAMA) and quercetin exposure (quercetin and isorhamnetin), were identified. In comparison with the control group, the intensities of GAMA, AAMA, iso-AAMA, 1-Salicylate Glucuronide, vinylacetylglycine, PE(20:1(11Z)/14:0), 7-ketodeoxycholic acid, cysteic acid, p-cresol sulfate, and l-cysteine in the AA-treated group were statistically significantly increased (p < 0.01), and the intensities of 2-indolecarboxylic acid, 3-acetamidobutanal, and kynurenic acid in the AA-treated group were statistically significantly decreased (p < 0.01). The above-mentioned metabolites were significantly ameliorated in the quercetin (50 mg per kg bw) plus AA-treated group compared with the AA-treated group (p < 0.01 or p < 0.05). However, the intensities of these metabolites in the quercetin (50 mg per kg bw) plus AA-treated groups were still significantly different from those of the control group (p < 0.01 or p < 0.05). The above results suggest that quercetin has a partial protective effect on AA-induced toxicity. The protective effects include regulation of fatty acid metabolism and amino acid metabolism and enhancing the antioxidant defense system.