Arachidonic Acid (sodium salt)
(Synonyms: 花生四烯酸钠,Sodium Arachidonate) 目录号 : GC42833A dietary ω-6 PUFA
Cas No.:6610-25-9
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
Polyunsaturated fatty acids (PUFAs) are essential nutrients that show distinct deficiency syndromes when not present in adequate amounts in the diet.[1][2] Virtually all cellular arachidonic acid is esterified in membrane phospholipids where its presence is tightly regulated through multiple interconnected pathways [3]. Free arachidonic acid is a transient, critical substrate for the biosynthesis of eicosanoid second messengers. Receptor-stimulated release, metabolism, and re-uptake of free arachidonate are all important aspects of cell signalling and inflammation.[4]
多不饱和脂肪酸（PUFAs）是必需营养素，在饮食中摄入不足时会表现出明显的缺乏综合症。几乎所有的细胞花生四烯酸都被酯化在膜磷脂中，其存在通过多个相互连接的途径进行严密调控。游离花生四烯酸是二级信使类前体，是瞬态的重要底物。受体刺激后的游离花生四烯酸的释放、代谢和重新摄取都是细胞信号传递和炎症的重要方面。
Reference:
[1]. Simopoulos, A.P. Omega-3 Fatty acids in health and disease and in growth and development. American Journal of Clinical Nutrition 54, 438-463 (1991).
[2]. Holman, R.T. Control of polyunsaturated acids in tissue lipids. J. Am. Coll. Nutr. 5(2), 183-211 (1986).
[3]. Nixon, A.B., Greene, D.G., and Wykle, R.L. Comparison of acceptor and donor substrates in the CoA-independent transacylase reaction in human neutrophils. Biochim. Biophys. Acta. 1300(3), 187-196 (1996).
[4]. Burgoyne, R.D., and Morgan, A. The control of free arachidonic acid levels. Trends Biochem. Sci. 15(10), 365-366 (1990).
| Cas No. | 6610-25-9 | SDF | |
| 别名 | 花生四烯酸钠,Sodium Arachidonate | ||
| 化学名 | 5Z,8Z,11Z,14Z-eicosatetraenoic acid, monosodium salt | ||
| Canonical SMILES | CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCC([O-])=O.[Na] | ||
| 分子式 | C20H31O2•Na | 分子量 | 326.5 |
| 溶解度 | Ethanol: 1 mg/ml, Ethanol:PBS (pH 7.2)(1:5): 0.5 mg/ml,Sodium Carbonate: 10 mg/ml | 储存条件 | Store at -20°C, protect from light |
| 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 | 3.0628 mL | 15.3139 mL | 30.6279 mL |
| 5 mM | 0.6126 mL | 3.0628 mL | 6.1256 mL |
| 10 mM | 0.3063 mL | 1.5314 mL | 3.0628 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。
The discovery and early structural studies of Arachidonic Acid
J Lipid Res 2016 Jul;57(7):1126-32.PMID:27142391DOI:10.1194/jlr.R068072.
Arachidonic Acid and esterified arachidonate are ubiquitous components of every mammalian cell. This polyunsaturated fatty acid serves very important biochemical roles, including being the direct precursor of bioactive lipid mediators such as prostaglandin and leukotrienes. This 20 carbon fatty acid with four double bonds was first isolated and identified from mammalian tissues in 1909 by Percival Hartley. This was accomplished prior to the advent of chromatography or any spectroscopic methodology (MS, infrared, UV, or NMR). The name, arachidonic, was suggested in 1913 based on its relationship to the well-known arachidic acid (C20:0). It took until 1940 before the positions of the four double bonds were defined at 5,8,11,14 of the 20-carbon chain. Total synthesis was reported in 1961 and, finally, the configuration of the double bonds was confirmed as all-cis-5,8,11,14. By the 1930s, the relationship of Arachidonic Acid within the family of essential fatty acids helped cue an understanding of its structure and the biosynthetic pathway. Herein, we review the findings leading up to the discovery of Arachidonic Acid and the progress toward its complete structural elucidation.
Intestinal Flora Modulates Blood Pressure by Regulating the Synthesis of Intestinal-Derived Corticosterone in High Salt-Induced Hypertension
Circ Res 2020 Mar 27;126(7):839-853.PMID:32078445DOI:10.1161/CIRCRESAHA.119.316394.
Rationale: High-salt diet is one of the most important risk factors for hypertension. Intestinal flora has been reported to be associated with high salt-induced hypertension (hSIH). However, the detailed roles of intestinal flora in hSIH pathogenesis have not yet been fully elucidated. Objective: To reveal the roles and mechanisms of intestinal flora in hSIH development. Methods and results: The abovementioned issues were investigated using various techniques including 16S rRNA gene sequencing, untargeted metabolomics, selective bacterial culture, and fecal microbiota transplantation. We found that high-salt diet induced hypertension in Wistar rats. The fecal microbiota of healthy rats could dramatically lower blood pressure (BP) of hypertensive rats, whereas the fecal microbiota of hSIH rats had opposite effects. The composition, metabolism, and interrelationship of intestinal flora in hSIH rats were considerably reshaped, including the increased corticosterone level and reduced Bacteroides and Arachidonic Acid levels, which tightly correlated with BP. The serum corticosterone level was also significantly increased in rats with hSIH. Furthermore, the above abnormalities were confirmed in patients with hypertension. The intestinal Bacteroides fragilis could inhibit the production of intestinal-derived corticosterone induced by high-salt diet through its metabolite Arachidonic Acid. Conclusions: hSIH could be transferred by fecal microbiota transplantation, indicating the pivotal roles of intestinal flora in hSIH development. High-salt diet reduced the levels of B fragilis and Arachidonic Acid in the intestine, which increased intestinal-derived corticosterone production and corticosterone levels in serum and intestine, thereby promoting BP elevation. This study revealed a novel mechanism different from inflammation/immunity by which intestinal flora regulated BP, namely intestinal flora could modulate BP by affecting steroid hormone levels. These findings enriched the understanding of the function of intestinal flora and its effects on hypertension.
Arachidonic Acid drives adaptive responses to chemotherapy-induced stress in malignant mesothelioma
J Exp Clin Cancer Res 2021 Nov 2;40(1):344.PMID:34727953DOI:10.1186/s13046-021-02118-y.
Background High resistance to therapy and poor prognosis characterizes malignant pleural mesothelioma (MPM). In fact, the current lines of treatment, based on platinum and pemetrexed, have limited impact on the survival of MPM patients. Adaptive response to therapy-induced stress involves complex rearrangements of the MPM secretome, mediated by the acquisition of a senescence-associated-secretory-phenotype (SASP). This fuels the emergence of chemoresistant cell subpopulations, with specific gene expression traits and protumorigenic features. The SASP-driven rearrangement of MPM secretome takes days to weeks to occur. Thus, we have searched for early mediators of such adaptive process and focused on metabolites differentially released in mesothelioma vs mesothelial cell culture media, after treatment with pemetrexed. Methods: Mass spectrometry-based (LC/MS and GC/MS) identification of extracellular metabolites and unbiased statistical analysis were performed on the spent media of mesothelial and mesothelioma cell lines, at steady state and after a pulse with pharmacologically relevant doses of the drug. ELISA based evaluation of Arachidonic Acid (AA) levels and enzyme inhibition assays were used to explore the role of cPLA2 in AA release and that of LOX/COX-mediated processing of AA. QRT-PCR, flow cytometry analysis of ALDH expressing cells and 3D spheroid growth assays were employed to assess the role of AA at mediating chemoresistance features of MPM. ELISA based detection of p65 and IkBalpha were used to interrogate the NFkB pathway activation in AA-treated cells. Results: We first validated what is known or expected from the mechanism of action of the antifolate. Further, we found increased levels of PUFAs and, more specifically, Arachidonic Acid (AA), in the transformed cell lines treated with pemetrexed. We showed that pharmacologically relevant doses of AA tightly recapitulated the rearrangement of cell subpopulations and the gene expression changes happening in pemetrexed -treated cultures and related to chemoresistance. Further, we showed that release of AA following pemetrexed treatment was due to cPLA2 and that AA signaling impinged on NFkB activation and largely affected anchorage-independent, 3D growth and the resistance of the MPM 3D cultures to the drug. Conclusions: AA is an early mediator of the adaptive response to pem in chemoresistant MPM and, possibly, other malignancies.
Safety and Efficacy of Sodium and Potassium Arachidonic Acid Salts in the Young Pig
Nutrients 2021 Apr 27;13(5):1482.PMID:33925724DOI:10.3390/nu13051482.
Arachidonic Acid (ARA; 20:4n6) and docosahexaenoic acid (DHA; 22:6n3) are polyunsaturated fatty acids (FA) naturally present in breast milk and added to most North American infant formulas (IF). We investigated the safety and efficacy of novel sodium and potassium salts of Arachidonic Acid as bioequivalent to support tissue levels of ARA comparable to the parent oil; M. alpina oil (Na-ARA and K-ARA) and including a Na-DHA group. Pigs of both sexes were randomized to one of five dietary treatments (n = 16 per treatment; 8 male and 8 female) from postnatal day 2 to 23. ARA and DHA were included as either triglyceride (TG) or salt. Target dietary ARA/DHA concentrations as percent of total FA by weight were as follows: TT (0.47 TG/0.32 TG), NaT (0.47 Na-salt/0.32 TG), KT (0.47 K-salt/0.32 TG), and Na0 (0.47 Na-salt/0.00), NaNa (0.47 Na-salt/0.32 Na-salt). The primary outcome in this study was bioequivalence of ARA brain accretion. Growth performance; blood and tissue fatty acid levels; liver histology; complete blood cell counts; and serum chemistries were all evaluated. Overall, diets containing test sources of ARA and DHA did not affect growth performance; liver histology; or substantially influence hematological outcomes as compared with TT. The results confirm that the use of Na and K salt forms of ARA yield bioequivalent ARA accretion in the cerebral cortex and retinal tissue compared to TG-ARA. These findings confirm that use of Na-ARA and K-ARA salts in the young pig was safe and nutritionally bioequivalent to TG-ARA for critical neural tissues.
Brain Arachidonic Acid uptake and turnover: implications for signaling and bipolar disorder
Curr Opin Clin Nutr Metab Care 2010 Mar;13(2):130-8.PMID:20145439DOI:10.1097/MCO.0b013e328336b615.
Purpose of review: Arachidonic Acid was first detected in the brain in 1922. Although earlier work examined the role of Arachidonic Acid in growth and development, more recent advancements have elucidated roles for Arachidonic Acid in brain health and disease. Recent findings: In this review, we summarize evidence demonstrating that unesterified Arachidonic Acid in the plasma pool, which is supplied in part from adipose, is readily taken up and incorporated into brain phospholipids. By labeling plasma unesterified Arachidonic Acid, it is possible to trace the subsequent release of Arachidonic Acid from brain phospholipids upon neuroreceptor-mediated release by phospholipase A2 in response to drugs and neuroinflammation in rodents. With the synthesis of 11C labeled fatty acids, brain Arachidonic Acid signaling can now be measured in humans with position emission tomography. Arachidonic Acid signals are known to regulate important biological functions, including neuroinflammation and excitotoxicity, and we focus on how the brain Arachidonic Acid cascade is a common target of drugs used to treat bipolar disorder (e.g. lithium, carbamazepine and valproate). Summary: A better understanding of the regulation of Arachidonic Acid uptake into the brain and the brain Arachidonic Acid cascade could lead to new imaging techniques and the identification of novel therapeutic targets in excitotoxicity, neuroinflammation and bipolar disorder.