Prostaglandin E2
(Synonyms: 前列腺素 E2; PGE2; Dinoprostone) 目录号 : GC15948
A primary COX product of arachidonic acid
Cas No.:363-24-6
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
| Cell experiment [1]: | |
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Cell lines |
Mouse bone-marrow-derived macrophages (BMMs) |
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Preparation Method |
BMMs were stimulated in complete RPMI supplemented with CSF-1 for indicated times with a combination of 20 ng/mL IL-4 , 10 μM prostaglandin E2, 100 μM 8-Br-cAMP, 20 μM Forskolin, 50 ng/mL IFN-γ, 20 ng/mL LPS, 100 μM Ap5a, 1.5 μM flurorcarbonyl cyanide phenylhydrazon, 10 nM valinomycin, 10 μM EdU, 10 μM KT5720, 10 μM H-89 or 2 μM α-amanitin under 5% CO2, atmospheric oxygen, at 37°C in a humidified incubator. |
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Reaction Conditions |
6h,10μM, 37°C |
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Applications |
Prostaglandin E2 induced the expression of some genes associated with alternative—M(IL-4)—cell activation including Arg1, Il4ra, and Clec10a (CD301), prostaglandin E2 accentuated IL-4-induced expression of Arg1, IL4ra, Clec10a, CD36, and Mrc1 when both stimuli where used simultaneously (co-stimulation), although it suppressed the expression of Retnla and Pparg, prostaglandin E2 did not alter IL-4-induced phosphorylation of STAT6. Thus, prostaglandin E2 has marked STAT6-independent effects on M(IL-4) cell activation. |
| Animal experiment [2]: | |
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Animal models |
Male Wistar rats (370-430 g) |
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Preparation Method |
Prostaglandin E2 was dissolved in heparin/saline (50 units/ml) and infused via the aortic cannula in a cumulative manner in doses ranging from 0.01-20 ug/min. Each dose was infused for a 5 min period. |
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Dosage form |
0.01ug/min-20ug/min, Prostaglandin E2 was dissolved in heparin/saline (50 units/ml) |
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Applications |
Dose-response curves demonstrate that under the conditions used, prostaglandin E2 produced a biphasic change in renal vascular resistance, vasodilatation started at 0.01 μg/min and was maximal at about 3 μg/min, while at the highest dose used (20μg/min) prostaglandin E2 induced renal vasoconstriction. |
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References: [1]. Sanin DE, Matsushita M, et,al. Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to Prostaglandin E2. Immunity. 2018 Dec 18;49(6):1021-1033.e6. doi: 10.1016/j.immuni.2018.10.011. PMID: 30566880; PMCID: PMC7271981. [2]. Haylor J, Towers J. Renal vasodilator activity of prostaglandin E2 in the rat anaesthetized with pentobarbitone. Br J Pharmacol. 1982 May;76(1):131-7. doi: 10.1111/j.1476-5381.1982.tb09198.x. PMID: 6952954; PMCID: PMC2068751. |
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Prostaglandin E2 is a major metabolite produced from arachidonic acid catalyzed by Cyclooxygenase (COX).It is also one of the most biologically active and widely studied prostaglandins. As a hormone-like substance that participate in a wide range of body functions such as the contraction and relaxation of smooth muscle, the dilation and constriction of blood vessels, control of blood pressure, and modulation of inflammation.?[4]
Mouse bone marrow derived na?ve macrophages produce prostaglandin E2 endogenously, resulting in anti-inflammatory gene expression upon differentiation induced by macrophage colony stimulating factor (M-CSF)[1].?Prostaglandin E2 has a mediator role for multiple inflammatory responses.?Prostaglandin E2 receptors EP1, EP2, EP3 and EP4, are involved in the regulation of prostaglandin E2-related processes, of which[5,6], EP2 and EP4 are closely associated with inflammatio.?EP2 and EP4 are involved in cytokine expression in E. coli-infected bovine endometrial tissue[7].?The affinity of PGE2 to these receptors varies according to the subtype and tissue type of the receptor, and the affinity constant (Kd) of prostaglandin E2 is about 1-10 nM. Prostaglandin E2 caused maximum relaxation of endothelin-1 precontracted vessels (EC50: 1.8×10-8M) [9].Prostaglandin E2-mediated enhancement of SPA expression in S. aureus-infected bovine endometrial tissue is dependent on EP4 receptor[4].PROSTAGLANDIN E2 induced the expression of some genes associated with alternative—M(IL-4)—cell activation including Arg1, Il4ra, and Clec10a (CD301), prostaglandin E2 accentuated IL-4-induced expression of Arg1, IL4ra, Clec10a, CD36, and Mrc1 when both stimuli where used simultaneously (co-stimulation), although it suppressed the expression of Retnla and Pparg, prostaglandin E2 did not alter IL-4-induced phosphorylation of STAT6.?Thus, prostaglandin E2 has marked STAT6-independent effects on M(IL-4) cell activation[3].
The effect of intra-aortic administration of prostaglandin E2 on renal blood flow was studied in the rat anaesthetized with pentobarbitone.?Dose-response curves demonstrate that under the conditions used, PROSTAGLANDIN E2 produced a biphasic change in renal vascular resistance, vasodilatation started at 0.01 μg/min and was maximal at about 3 μg/min, while at the highest dose used (20μg/min) prostaglandin E2 induced renal vasoconstriction[2].In addition, prostaglandin E2 have been shown to have complex effects on skeletal tissues, but a major effect in vivo is to increase both bone formation and bone resorption or bone remodeling, In a study in rats continuous infusion of prostaglandin E2 produced net bone loss while daily injection led to net bone gain[8].
References:
[1]: Na YR, Jung D, et,al. Endogenous prostaglandin E2 potentiates anti-inflammatory phenotype of macrophage through the CREB-C/EBP-β cascade. Eur J Immunol. 2015 Sep;45(9):2661-71. doi: 10.1002/eji.201545471. Epub 2015 Jul 20. PMID: 26118414.
[2]: Haylor J, Towers J. Renal vasodilator activity of prostaglandin E2 in the rat anaesthetized with pentobarbitone. Br J Pharmacol. 1982 May;76(1):131-7. doi: 10.1111/j.1476-5381.1982.tb09198.x. PMID: 6952954; PMCID: PMC2068751.
[3]: Sanin DE, Matsushita M, et,al. Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to Prostaglandin E2. Immunity. 2018 Dec 18;49(6):1021-1033.e6. doi: 10.1016/j.immuni.2018.10.011. PMID: 30566880; PMCID: PMC7271981.
[4]: Liu K, Mao W, et,al. Prostaglandin E2 promotes Staphylococcus aureus infection via EP4 receptor in bovine endometrium. Microb Pathog. 2021 Sep;158:105019. doi: 10.1016/j.micpath.2021.105019. Epub 2021 Jun 6. PMID: 34107344.
[5]: Wu J, Liu B, et,al. Prostaglandin E2 Regulates Activation of Mouse Peritoneal Macrophages by Staphylococcus aureus through Toll-Like Receptor 2, Toll-Like Receptor 4, and NLRP3 Inflammasome Signaling. J Innate Immun. 2020;12(2):154-169. doi: 10.1159/000499604. Epub 2019 May 29. PMID: 31141808; PMCID: PMC7098297.
[6]: Li T, Liu B, et,al. PGE2 increases inflammatory damage in Escherichia coli-infected bovine endometrial tissue in vitro via the EP4-PKA signaling pathway. Biol Reprod. 2019 Jan 1;100(1):175-186. doi: 10.1093/biolre/ioy162. PMID: 30010723.
[7]: Zhang C, Wang L, et,al. EP2/4 Receptors Promote the Synthesis of PGE2 Increasing Tissue Damage in Bovine Endometrial Explants Induced by?Escherichia coli. J Pharmacol Exp Ther. 2020 Feb;372(2):175-184. doi: 10.1124/jpet.119.262444. Epub 2019 Nov 15. PMID: 31732699.
[8]: Tian XY, Zhang Q, et,al. Continuous PGE2 leads to net bone loss while intermittent PGE2 leads to net bone gain in lumbar vertebral bodies of adult female rats. Bone. 2008 May;42(5):914-20. doi: 10.1016/j.bone.2007.12.228. Epub 2008 Feb 5. PMID: 18316259.
[9]:Astin M, Stjernschantz J. Mechanism of prostaglandin E2-, F2alpha- and latanoprost acid-induced relaxation of submental veins. Eur J Pharmacol. 1997 Dec 11;340(2-3):195-201. doi: 10.1016/s0014-2999(97)01414-3. PMID: 9537815.
前列腺素 E2 是由花生四烯酸在环氧合酶 (COX) 催化下产生的主要代谢产物。它也是最具生物活性和研究最广泛的前列腺素之一。作为一种激素样物质，参与广泛的身体功能，如平滑肌的收缩和松弛、血管的扩张和收缩、血压的控制和炎症的调节。 [4]
源自小鼠骨髓的幼稚巨噬细胞内源性产生前列腺素 E2，从而在巨噬细胞集落刺激因子 (M-CSF) 诱导的分化过程中产生抗炎基因表达[1]。前列腺素 E2 对多种炎症反应具有调节作用。前列腺素E2受体EP1、EP2、EP3和EP4参与前列腺素E2相关过程的调控，其中[5,6]、EP2和EP4与炎症密切相关。 EP2和EP4参与大肠杆菌感染的牛子宫内膜组织中细胞因子的表达[7]。 PGE2对这些受体的亲和力根据受体亚型和组织类型的不同而不同，前列腺素E2的亲和常数(Kd)约为1-10 nM。前列腺素E2引起endothelin-1预收缩血管的最大松弛（EC50:1.8×10-8M）[9]。前列腺素E2介导的S.SPA表达增强。金黄色葡萄球菌感染的牛子宫内膜组织依赖于 EP4 受体[4]。前列腺素 E2 诱导了一些与替代性 M(IL-4) 细胞激活相关的基因的表达，包括 Arg1、Il4ra 和 Clec10a (CD301)，当同时使用两种刺激物（共刺激）时，前列腺素 E2 会增强 IL-4 诱导的 Arg1、IL4ra、Clec10a、CD36 和 Mrc1 的表达，尽管它会抑制 Retnla 和 Pparg 的表达，但前列腺素 E2 不会改变 IL-4 诱导的 STAT6 磷酸化。因此，前列腺素E2对M(IL-4)细胞活化具有显着的STAT6非依赖性作用[3]。
在用戊巴比妥麻醉的大鼠中研究了主动脉内施用前列腺素 E2 对肾血流量的影响。剂量反应曲线表明，在所用条件下，前列腺素 E2 会在肾血管阻力方面产生双相变化，血管舒张在 0.01 微克/分钟时开始，在约 3 微克/分钟时达到最大，而在使用的最高剂量（20 微克/分钟）时前列腺素 E2 诱导肾血管收缩[2]。此外，前列腺素 E2 已被证明对骨骼组织具有复杂的作用，但在体内的主要作用是增加骨形成和骨吸收或骨重塑, 在一项针对大鼠的研究中，连续输注前列腺素 E2 会导致净骨质流失，而每日注射会导致净骨质增加[8]。
| Cas No. | 363-24-6 | SDF | |
| 别名 | 前列腺素 E2; PGE2; Dinoprostone | ||
| 化学名 | (Z)-7-((1R,2R,3R)-3-hydroxy-2-((S,E)-3-hydroxyoct-1-en-1-yl)-5-oxocyclopentyl)hept-5-enoic acid | ||
| Canonical SMILES | O[C@H](C1)[C@H](/C=C/[C@H](CCCCC)O)[C@@H](C/C=C\CCCC(O)=O)C1=O | ||
| 分子式 | C20H32O5 | 分子量 | 352.47 |
| 溶解度 | 70 mg/mL (198.60 mM) in DMSO, 70 mg/mL (198.60 mM) in Ethanol | 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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.8371 mL | 14.1856 mL | 28.3712 mL |
| 5 mM | 0.5674 mL | 2.8371 mL | 5.6742 mL |
| 10 mM | 0.2837 mL | 1.4186 mL | 2.8371 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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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，
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2.
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Prostaglandin E2 synthesis and secretion: the role of PGE2 synthases
Clin Immunol2006 Jun;119(3):229-40.PMID: 16540375DOI: 10.1016/j.clim.2006.01.016
Prostaglandin E2 (PGE2) is a principal mediator of inflammation in diseases such as rheumatoid arthritis and osteoarthritis. Nonsteroidal anti-inflammatory medications (NSAIDs) and selective cyclooxygenase-2 (COX-2) inhibitors reduce PGE2 production to diminish the inflammation seen in these diseases, but have toxicities that may include both gastrointestinal bleeding and prothrombotic tendencies. In cells, arachidonic acid is transformed into PGE2 via cyclooxygenase (COX) enzymes and terminal prostaglandin E synthases (PGES). Accumulating data suggest that the interaction of various enzymes in the PGE2 synthetic pathway is complex and tightly regulated. In this review, we summarize the synthesis and secretion of PGE2. In particular, we focus on the three isoforms of the terminal PGES, and discuss the potential of targeting PGES as a more precise strategy for inhibiting PGE2 production.
Role of prostaglandin E2 in tissue repair and regeneration
Theranostics2021 Aug 13;11(18):8836-8854.PMID: 34522214DOI: 10.7150/thno.63396
Tissue regeneration following injury from disease or medical treatment still represents a challenge in regeneration medicine. Prostaglandin E2 (PGE2), which involves diverse physiological processes via E-type prostanoid (EP) receptor family, favors the regeneration of various organ systems following injury for its capabilities such as activation of endogenous stem cells, immune regulation, and angiogenesis. Understanding how PGE2 modulates tissue regeneration and then exploring how to elevate the regenerative efficiency of PGE2 will provide key insights into the tissue repair and regeneration processes by PGE2. In this review, we summarized the application of PGE2 to guide the regeneration of different tissues, including skin, heart, liver, kidney, intestine, bone, skeletal muscle, and hematopoietic stem cell regeneration. Moreover, we introduced PGE2-based therapeutic strategies to accelerate the recovery of impaired tissue or organs, including 15-hydroxyprostaglandin dehydrogenase (15-PGDH) inhibitors boosting endogenous PGE2 levels and biomaterial scaffolds to control PGE2 release.
Prostaglandin E2 involvement in mammalian female fertility: ovulation, fertilization, embryo development and early implantation
Reprod Biol Endocrinol2018 May 1;16(1):43.PMID: 29716588DOI: 10.1186/s12958-018-0359-5
Background: Infertility in mammalian females has been a challenge in reproductive medicine. The causes of female infertility include anovulation, ovulated oocyte defects, abnormal fertilization, and insufficient luteal support for embryo development, as well as early implantation. Ovulation induction, in vitro fertilization and luteal support regimens have been performed for decades to increase fertility rates. The identification of proteins and biochemical factors involved in female reproduction is essential to further increase female fertility rates. Evidence has shown that prostaglandins (PGs) might be involved in the female reproductive process, mainly ovulation, fertilization, and implantation. However, only a few studies on individual PGs in female reproduction have been done so far. This review aimed to identify the pivotal role of prostaglandin E2 (PGE2), a predominant PG, in female reproduction to improve fertility, specifically ovulation, fertilization, embryo development and early implantation.
Results: Prostaglandin E2 (PGE2) was shown to play a relevant role in the ovulatory cascade, including meiotic maturation, cumulus expansion and follicle rupture, through inducing ovulatory genes, such as Areg, Ereg, Has2 and Tnfaip6, as well as increasing intracellular cAMP levels. PGE2 reduces extracellular matrix viscosity and thereby optimizes the conditions for sperm penetration. PGE2 reduces the phagocytic activity of polymorphonuclear neutrophils (PMNs) against sperm. In the presence of PGE2, sperm function and binding capacity to oocytes are enhanced. PGE2 maintains luteal function for embryo development and early implantation. In addition, it induces chemokine expression for trophoblast apposition and adhesion to the decidua for implantation.
Conclusion: It has been shown that PGE2 positively affects different stages of female fertility. Therefore, PGE2 should be taken into consideration when optimizing reproduction in infertile females. We suggest that in clinical practice, the administration of non-steroidal anti-inflammatory drugs, which are PGE2 synthesis inhibitors, should be reasonable and limited in infertile women. Additionally, assessments of PGE2 protein and receptor expression levels should be taken into consideration.
[Role of prostaglandin E2 receptor 4 in cardiovascular diseases]
Sheng Li Xue Bao2019 Apr 25;71(2):361-370.PMID: 31008497DOI: 10.3760/cma.j.cn501113-20190422-00140
Prostaglandin E2 (PGE2) is a cyclooxygenase metabolite of arachidonic acid. It acts as a bioactive lipid and plays an important role in regulating many biological processes. PGE2 binds to 4 different G protein-coupled receptors including prostaglandin E2 receptor subtypes EP1, EP2, EP3 and EP4. The EP4 receptor is widely expressed in most of human organs and tissues. Increasing evidence demonstrates that EP4 is essential for cardiovascular homeostasis and participates in the pathogenesis of many cardiovascular diseases. Here we summarize the role of EP4 in the regulation of cardiovascular function and discuss potential mechanisms by which EP4 is involved in the development of cardiovascular disorders with a focus on its effect on inflammation.
[Metabolism and transport pathway of prostaglandin E2 and its role in liver regeneration]
Zhonghua Gan Zang Bing Za Zhi2021 Feb 20;29(2):183-187.PMID: 33685091DOI: 10.3760/cma.j.cn501113-20190422-00140
The liver is an organ with regenerative capacity and is essential for maintaining the body homeostasis. Under pathological conditions, such as chronic hepatitis, liver cirrhosis and so on, the impairment of liver regeneration can lead to insufficient liver function or even liver failure. Therefore, promoting liver regeneration can improve the patient's prognosis. Prostaglandin E2 is a hormone-like messenger with physiological activity that can promote tissue regeneration. This article reviews the metabolism and transport pathways of prostaglandin E2 and its mechanism of action in liver tissue regeneration, and proposes that prostaglandin E2 is an important cytokine involved in the liver regeneration process, and has potential clinical application prospects for the treatment of liver injury.