Arachidonic acid (Immunocytophyt)
(Synonyms: 花生四烯酸; Immunocytophyt) 目录号 : GC31725
花生四烯酸Arachidonic acid 是一种必需的不饱和脂肪酸,存在于动物和人类脂肪中,也存在于肝脏、大脑和腺体器官中。
Cas No.:506-32-1
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
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- Datasheet
| Cell experiment [1]: | |
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Cell lines |
Embryoid bodies (EBs) |
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Preparation Method |
Embryoid bodies (EBs) were seeded in 24-well plates and treated with various concentrations of Arachidonic acid alone, Valproic acid (VA) alone and VA in combination with 3.3 µM Arachidonic acid. |
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Reaction Conditions |
3.3µM;24h |
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Applications |
Arachidonic acid supports EB formation and protects EBs from Valproic acid (VA)-induced embryotoxicity. |
| Animal experiment [2]: | |
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Animal models |
Swiss Albino male mice (feeding high-fat diets to induce obesity) |
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Preparation Method |
Mice groups were divided into three groups. Two groups of mice received two different doses of AA, which were 1 mg/kg of body weight named Low Arachidonic Acid (LAA) and 4 mg/kg of body weight named Moderate Arachidonic Acid (MAA) once daily through oral gavage, along with HFD(high-fat diets). The remaining obese group of mice was continued with HFD. |
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Dosage form |
1-4mg/kg; i.g; once daily for 3weeks |
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Applications |
Arachidonic acid treatment has resulted in a significant down-regulation of pro-inflammatory markers as well as the COX pathway in obesity mice. |
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References: [1]. Nihad M, Sen U, et,al. Arachidonic acid modulates the cellular energetics of human pluripotent stem cells and protects the embryoid bodies from embryotoxicity effects in vitro. Reprod Toxicol. 2023 Sep;120:108438. doi: 10.1016/j.reprotox.2023.108438. Epub 2023 Jul 16. PMID: 37454977. |
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Arachidonic acid is an essential unsaturated fatty acid, found in animal and human fats, as well as in liver, brain and glandular organs. It is one of the phospholipids in animals. It is a precursor to the biosynthesis of prostaglandins and leukotrienes. Arachidonic acid is an important factor in cell signaling and the occurrence of inflammation[1-3].
Arachidonic acid(0-40 µM; 3min) stimulates protein tyrosine phosphorylation in vascular cells[4]. Arachidonic acid (3.3µM;24h) supports EB formation and protects EBs from Valproic acid (VA)-induced embryotoxicity[5].
Arachidonic acid (1-4mg/kg; i.g.; once daily for 3weeks) treatment has resulted in a significant down-regulation of pro-inflammatory markers as well as the COX pathway and up-regulation of 12/15-LOX has been observed in obesity mice[6].Arachidonic acid+ diet could prevent amyloid β-protein (Aβ) deposition through the alteration of amyloid precursor protein (APP) processing in Tg2576 mice[7].
References:
[1]. Tallima H, El Ridi R. Arachidonic acid: Physiological roles and potential health benefits - A review. J Adv Res. 2017 Nov 24;11:33-41. doi: 10.1016/j.jare.2017.11.004. PMID: 30034874; PMCID: PMC6052655.
[2]. Wang B, Wu L,et,al. Metabolism pathways of arachidonic acids: mechanisms and potential therapeutic targets. Signal Transduct Target Ther. 2021 Feb 26;6(1):94. doi: 10.1038/s41392-020-00443-w. PMID: 33637672; PMCID: PMC7910446.
[3]. Turolo S, Edefonti A, et,al. Role of Arachidonic Acid and Its Metabolites in the Biological and Clinical Manifestations of Idiopathic Nephrotic Syndrome. Int J Mol Sci. 2021 May 21;22(11):5452. doi: 10.3390/ijms22115452. PMID: 34064238; PMCID: PMC8196840.
[4]. Buckley BJ, Whorton AR. Arachidonic acid stimulates protein tyrosine phosphorylation in vascular cells. Am J Physiol. 1995 Dec;269(6 Pt 1):C1489-95. doi: 10.1152/ajpcell.1995.269.6.C1489. PMID: 8572178.
[5]. Nihad M, Sen U, et,al. Arachidonic acid modulates the cellular energetics of human pluripotent stem cells and protects the embryoid bodies from embryotoxicity effects in vitro. Reprod Toxicol. 2023 Sep;120:108438. doi: 10.1016/j.reprotox.2023.108438. Epub 2023 Jul 16. PMID: 37454977.
[6]. Roy S, Ripon MAR, et,al. Arachidonic acid supplementation attenuates adipocyte inflammation but not adiposity in high fat diet induced obese mice. Biochem Biophys Res Commun. 2022 Jun 11;608:90-95. doi: 10.1016/j.bbrc.2022.03.089. Epub 2022 Mar 29. PMID: 35397428.
[7]. Hosono T, Nishitsuji K, et,al. Arachidonic acid diet attenuates brain Aβ deposition in Tg2576 mice. Brain Res. 2015 Jul 10;1613:92-9. doi: 10.1016/j.brainres.2015.04.005. Epub 2015 Apr 13. PMID: 25881896.
花生四烯酸Arachidonic acid 是一种必需的不饱和脂肪酸,存在于动物和人类脂肪中,也存在于肝脏、大脑和腺体器官中。它是动物体内磷脂的一种。它是前列腺素和白三烯生物合成的前体。花生四烯酸也是细胞信号传导和炎症发生的重要因子[1-3]。
花生四烯酸(0-40 µM; 3min)刺激血管细胞中的蛋白酪氨酸磷酸化[4]。花生四烯酸 (3.3µM;24h)支持胚状体形成并保护胚状体免受丙戊酸(VA)诱导的胚胎毒性[5]。
花生四烯酸处理(1-4mg/kg; i.g.; once daily for 3weeks)导致肥胖小鼠的促炎标志物和COX通路显著下调,12/15-LOX上调[6]。花生四烯酸饮食可通过改变Tg2576小鼠的淀粉样前体蛋白(APP)加工来阻止淀粉样β蛋白Aβ沉积[7]。
| Cas No. | 506-32-1 | SDF | |
| 别名 | 花生四烯酸; Immunocytophyt | ||
| Canonical SMILES | CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCC(O)=O | ||
| 分子式 | C20H32O2 | 分子量 | 304.47 |
| 溶解度 | DMSO : ≥ 50 mg/mL (164.22 mM);Ethanol : ≥ 50 mg/mL (164.22 mM);Water : < 0.1 mg/mL (insoluble) | 储存条件 | -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 | 3.2844 mL | 16.422 mL | 32.844 mL |
| 5 mM | 0.6569 mL | 3.2844 mL | 6.5688 mL |
| 10 mM | 0.3284 mL | 1.6422 mL | 3.2844 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 Role of Arachidonic and Linoleic Acid Derivatives in Pathological Pregnancies and the Human Reproduction Process
The aim of the available literature review was to focus on the role of the proinflammatory mediators of AA and LA derivatives in pathological conditions related to reproduction and pregnancy. Arachidonic (AA) and linoleic acid (LA) derivatives play important roles in human fertility and the course of pathological pregnancies. Recent studies have demonstrated that uncontrolled inflammation has a significant impact on reproduction, spermatogenesis, endometriosis, polycystic ovary syndrome (PCOS) genesis, implantation, pregnancy and labor. In addition, cyclooxygenase-mediated prostaglandins and AA metabolite levels are higher in women's ovarian tissue when suffering from PCOS. It has been demonstrated that abnormal cyclooxygenase-2 (COX-2) levels are associated with ovulation failure, infertility, and implantation disorders and the increase in 9-HODE/13-HODE was a feature recognized in PCOS patients. Maintaining inflammation without neutrophil participation allows pregnant women to tolerate the fetus, while excessive inflammatory activation may lead to miscarriages and other pathological complications in pregnancies. Additionally AA and LA derivatives play an important role in pregnancy pathologies, e.g., gestational diabetes mellitus, preeclampsia (PE), and fetal growth, among others. The pathogenesis of PE and other pathological states in pregnancy involving eicosanoids have not been fully identified. A significant expression of 15-LOX-1,2 was found in women with PE, leading to an increase in the synthesis of AA and LA derivatives, such as hydroxyeicozatetraenoic acids (HETE) and hydroxyoctadecadiene acids (HODE). Synthesis of the metabolites 5-, 8-, 12-, and 15-HETE increased in the placenta, while 20-HETE increased only in umbilical cord blood in women with preeclampsia compared to normal pregnancies. In obese women with gestational diabetes mellitus (GDM) an increase in epoxygenase products in the cytochrome P450 (CYP) and the level of 20-HETE associated with the occurrence of insulin resistance (IR) were found. In addition, 12- and 20-HETE levels were associated with arterial vasoconstriction and epoxyeicosatrienoic acids (EETs) with arterial vasodilatation and uterine relaxation. Furthermore, higher levels of 5- and 15-HETE were associated with premature labor. By analyzing the influence of free fatty acids (FFA) and their derivatives on male reproduction, it was found that an increase in the AA in semen reduces its amount and the ratio of omega-6 to omega-3 fatty acids showed higher values in infertile men compared to the fertile control group. There are several studies on the role of HETE/HODE in relation to male fertility. 15-Hydroperoxyeicosatetraenoic acid may affect the integrity of the membrane and sperm function. Moreover, the incubation of sperm with physiologically low levels of prostaglandins (PGE2/PGF2α) improves the functionality of human sperm. Undoubtedly, these problems are still insufficiently understood and require further research. However, HETE and HODE could serve as predictive and diagnostic biomarkers for pregnancy pathologies (especially in women with risk factors for overweight and obesity). Such knowledge may be helpful in finding new treatment strategies for infertility and the course of high-risk pregnancies.
The discovery and early structural studies of arachidonic acid
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.
Arachidonic acid drives adaptive responses to chemotherapy-induced stress in malignant mesothelioma
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.
Brain arachidonic acid uptake and turnover: implications for signaling and bipolar disorder
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.