Resolvin E1
(Synonyms: RvE1) 目录号 : GC40612A specialized pro-resolving mediator
Cas No.:552830-51-0
Sample solution is provided at 25 µL, 10mM.
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Resolvin E1 (RvE1) is a trihydroxy eicosapentaenoic acid metabolite that has been identified in mouse inflammatory exudates and in human plasma when subjects are treated with both aspirin and supplemental EPA.[1],[2],[3] RvE1 is an anti-inflammatory EPA metabolite that has been shown to promote inflammatory resolution in numerous disease models, including experimental colitis, asthma, atherosclerosis, type 2 diabetes, and HSV-1-induced stromal keratitis.[4],[5],[6],[7],[8],[9],[10],[11]
Resolvin E1（RvE1）是一种三羟基二十碳五烯酸代谢物，在小鼠炎症渗出物和人类血浆中已被鉴定，当受试者同时接受阿司匹林和补充的EPA时可发现RvE1的存在。RvE1是一种抗炎EPA代谢产物，已被证明在多种疾病模型中促进炎症的解决，包括实验性结肠炎，哮喘，动脉粥样硬化，2型糖尿病和HSV-1引起的角膜炎
Reference:
[1]. Serhan, C.N., Clish, C.B., Brannon, J., et al. Novel functional sets of lipid-derived mediators with antiinflammatory actions generated from omega-3 fatty acids via cyclooxygenase 2-nonsteroidal antiinflammatory drugs and transcellular processing. Journal of Experimental Medicine 192(8), 1197-1204 (2000).
[2]. Serhan, C.N., Hong, S., Gronert, K., et al. Resolvins: A family of bioactive products of ω-3 fatty acid transformation circuits by aspirin treatment that counter proinflammation signals. J. Exp. Med. 196(8), 1025-1037 (2002).
[3]. Arita, M., Bianchini, F., Aliberti, J., et al. Sterochemical assignment, antiinflammatory properties, and receptor for the omega-3 lipid mediator resolvin E1. Journal of Experimental Medicine 201(5), 713-722 (2005).
[4]. Flower, R.J., and Perretti, M. Controlling inflammation: A fat chance? Journal of Experimental Biology 201(5), 671-674 (2005).
[5]. Arita, M., Yoshida, M., Hong, S., et al. Resolvin E1, an endogenous lipid mediator derived from omega-3 eicosapentaenoic acid, protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis. Proceedings of the National Academy of Sciences of the United States of America 102(21), 7671-7676 (2005).
[6]. Aoki, H., Hisada, T., Ishizuka, T., et al. Resolvin E1 dampens airway inflammation and hyperresponsiveness in a murine model of asthma. Biochemical and Biophysical Research Communications 367, 509-515 (2008).
[7]. Haworth, O., Cernadas, M., and Levy, B.D. NK cells are effectors for resolvin E1 in the timely resolution of allergic airway inflammation. Journal of Immunology 186(11), 6129-6135 (2011).
[8]. Campbell, E.K., MacManus, C.F., Kominsky, D.J., et al. Resolvin E1-induced intestinal alkaline phosphatase promotes resolution of inflammation through LPS detoxification. Proceedings of the National Academy of Sciences of the United States of America 107(32), 14298-14303 (2010).
[9]. Hasturk, H., Abdallah, R., Kantarck, A., et al. Resolvin E1 (RvE1) attenuates atherosclerotic plaque formation in diet and inflammation-induced atherogenesis. Arteriosclerosis, Thrombosis, and Vascular Biology 35(5), 1123-1133 (2015).
[10]. Herrera, N.S., Hasturk, H., Kantarck, A., et al. Impact of resolvin E1 on murine neutrophil phagocytosis in type 2 diabetes. Infection and Immunity 83(2), 792-801 (2015).
[11]. Rajasagi, N.K., Reddy, P.B.J., Suryawanshi, A., et al. Controlling herpes simplex virus-induced ocular inflammatory lesions with the lipid-derived mediator resolvin E1. Journal of Immunology 186(3), 1735-1746 (2011).
| Cas No. | 552830-51-0 | SDF | |
| 别名 | RvE1 | ||
| 化学名 | 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid | ||
| Canonical SMILES | O[C@@H](CCCC(O)=O)/C=C\C=C\C=C\[C@H](O)C/C=C\C=C\[C@H](O)CC | ||
| 分子式 | C20H30O5 | 分子量 | 350.5 |
| 溶解度 | 50 mg/ml in DMF, 50 mg/ml in Ethanol | 储存条件 | Store at -80°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 | 2.8531 mL | 14.2653 mL | 28.5307 mL |
| 5 mM | 0.5706 mL | 2.8531 mL | 5.7061 mL |
| 10 mM | 0.2853 mL | 1.4265 mL | 2.8531 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。
Resolvin E1 Attenuates Pulmonary Hypertension by Suppressing Wnt7a/β-Catenin Signaling
Hypertension 2021 Dec;78(6):1914-1926.PMID:34689593DOI:10.1161/HYPERTENSIONAHA.121.17809.
[Figure: see text].
Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis
Circulation 2020 Aug 25;142(8):776-789.PMID:32506925DOI:10.1161/CIRCULATIONAHA.119.041868.
Background: Aortic valve stenosis (AVS), which is the most common valvular heart disease, causes a progressive narrowing of the aortic valve as a consequence of thickening and calcification of the aortic valve leaflets. The beneficial effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs) in cardiovascular prevention have recently been demonstrated in a large randomized, controlled trial. In addition, n-3 PUFAs serve as the substrate for the synthesis of specialized proresolving mediators, which are known by their potent beneficial anti-inflammatory, proresolving, and tissue-modifying properties in cardiovascular disease. However, the effects of n-3 PUFA and specialized proresolving mediators on AVS have not yet been determined. The aim of this study was to identify the role of n-3 PUFA-derived specialized proresolving mediators in relation to the development of AVS. Methods: Lipidomic and transcriptomic analyses were performed in human tricuspid aortic valves. Apoe-/- mice and wire injury in C57BL/6J mice were used as models for mechanistic studies. Results: We found that n-3 PUFA incorporation into human stenotic aortic valves was higher in noncalcified regions compared with calcified regions. Liquid chromatography tandem mass spectrometry-based lipid mediator lipidomics identified that the n-3 PUFA-derived specialized proresolving mediator Resolvin E1 was dysregulated in calcified regions and acted as a calcification inhibitor. Apoe-/- mice expressing the Caenorhabditis elegans Fat-1 transgene (Fat-1tg×Apoe-/-), which enables the endogenous synthesis of n-3 PUFA and increased valvular n-3 PUFA content, exhibited reduced valve calcification, lower aortic valve leaflet area, increased M2 macrophage polarization, and improved echocardiographic parameters. Finally, abrogation of the Resolvin E1 receptor ChemR23 enhanced disease progression, and the beneficial effects of Fat-1tg were abolished in the absence of ChemR23. Conclusions: n-3 PUFA-derived Resolvin E1 and its receptor ChemR23 emerge as a key axis in the inhibition of AVS progression and may represent a novel potential therapeutic opportunity to be evaluated in patients with AVS.
Resolvin E1 accelerates pulp repair by regulating inflammation and stimulating dentin regeneration in dental pulp stem cells
Stem Cell Res Ther 2021 Jan 22;12(1):75.PMID:33482900DOI:10.1186/s13287-021-02141-y.
Background: Unresolved inflammation and tissue destruction are considered to underlie the failure of dental pulp repair. As key mediators of the injury response, dental pulp stem cells (DPSCs) play a critical role in pulp tissue repair and regeneration. Resolvin E1 (RvE1), a major dietary omega-3 polyunsaturated fatty-acid metabolite, is effective in resolving inflammation and activating wound healing. However, whether RvE1 facilitates injured pulp-tissue repair and regeneration through timely resolution of inflammation and rapid mobilization of DPSCs is unknown. Therefore, we established a pulp injury model and investigated the effects of RvE1 on DPSC-mediated inflammation resolution and injured pulp repair. Methods: A pulp injury model was established using 8-week-old Sprague-Dawley rats. Animals were sacrificed on days 1, 3, 7, 14, 21, and 28 after pulp capping with a collagen sponge immersed in PBS with RvE1 or PBS. Hematoxylin-eosin and Masson's trichrome staining, immunohistochemistry, and immunohistofluorescence were used to evaluate the prohealing properties of RvE1. hDPSCs were incubated with lipopolysaccharide (LPS) to induce an inflammatory response, and the expression of inflammatory factors after RvE1 application was measured. Effects of RvE1 on hDPSC proliferation, chemotaxis, and odontogenic differentiation were evaluated by CCK-8 assay, transwell assay, alkaline phosphatase (ALP) staining, alizarin red staining, and quantitative PCR, and possible signaling pathways were explored using western blotting. Results: In vivo, RvE1 reduced the necrosis rate of damaged pulp and preserved more vital pulps, and promoted injured pulp repair and reparative dentin formation. Further, it enhanced dentin matrix protein 1 and dentin sialoprotein expression and accelerated pulp inflammation resolution by suppressing TNF-α and IL-1β expression. RvE1 enhanced the recruitment of CD146+ and CD105+ DPSCs to the damaged molar pulp mesenchyme. Isolated primary cells exhibited the mesenchymal stem cell immunophenotype and differentiation. RvE1 promoted hDPSC proliferation and chemotaxis. RvE1 significantly attenuated pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) release and enhanced ALP activity, nodule mineralization, and especially, expression of the odontogenesis-related genes DMP1, DSPP, and BSP in LPS-stimulated DPSCs. RvE1 regulated AKT, ERK, and rS6 phosphorylation in LPS-stimulated DPSCs. Conclusions: RvE1 promotes pulp inflammation resolution and dentin regeneration and positively influences the proliferation, chemotaxis, and differentiation of LPS-stimulated hDPSCs. This response is, at least partially, dependent on AKT, ERK, and rS6-associated signaling in the inflammatory microenvironment. RvE1 has promising application potential in regenerative endodontics.
Resolvin E1's Antimicrobial Potential Against Aggregatibacter Actinomycetemcomitans
Front Oral Health 2022 Apr 27;3:875047.PMID:35571980DOI:10.3389/froh.2022.875047.
Background: Microorganisms along with host response play a key role in the development of periodontal and peri-implant infections. Advanced periodontal and peri-implant diseases are most likely associated with bacterial plaques that trigger host immune response and eventually lead to the destruction of the attachment apparatus and bone loss around a tooth or a dental implant. A recent systematic review and meta-analysis revealed that Aggregatibacter actinomycetemcomitans had the highest association with peri-implantitis. Resolvin E1 (RvE1) is part of the specialized pro-resolving lipid mediator family biosynthesized from omega-3, polyunsaturated fatty acids (PUFAs), and eicosapentaenoic acid (EPA). Although RvE1 is an established anti-inflammatory agent, it was found that its application as a treatment or as a preventive drug had an indirect effect on the subgingival microbiota of both rats and rabbits with experimental periodontitis. Aim: The aim of this study is to evaluate the direct antimicrobial effect of RvE1 on Aggregatibacter actinomycetemcomitans bacteria. Materials and methods: The study comprised three groups that underwent minimum inhibitory concentration (MIC) against Aggregatibacter actinomycetemcomitans. The first group was tested with the RvE1 working concentration of 5 ug/ml, the second group was tested with ethanol (EtOH), 10% as the working concentration, and the final group was diluted in phosphate-buffered saline (PBS) as the positive control. Optical density (OD600) was used for the comparison of bacterial growth among the tested groups. The experiment was conducted in three biological replicates. Data were analyzed using SPSS, and results were analyzed by using one-way analysis of variance (ANOVA) followed by post-hoc Bonferroni using a minimum level of significance (P-value) of 0.05. Results: Minimum inhibitory concentration was 1.25 μg/ml and 5% for RvE1 and EtOH, respectively. RvE1's mean optical density (OD600) was 0.156 ± 0.021 and was significantly lower compared with all the other groups (P-value < 0.01). The EtOH group (mean OD600 0.178 ± 0.013) and the PBS group (mean OD600 0.1855 ± 0.022) did not reveal a significant difference (P-value = 0.185). Conclusion: RvE1 demonstrated significant antimicrobial activity against A. actinomycetemcomitans with an MIC of 1.25 μg/ml. The RvE1 group showed significantly lower bacterial growth compared to the EtOH and PBS groups.
Resolvin E1 as a novel agent for the treatment of asthma
Expert Opin Ther Targets 2009 May;13(5):513-22.PMID:19368495DOI:10.1517/14728220902865622.
Background: Asthma is characterized by airway hyperresponsiveness and chronic airway inflammation. Inflammatory cells, including eosinophils and lymphocytes, infiltrate peribronchial tissue in patients with asthma. Resolvin E1 (RvE1) is an anti-inflammatory lipid mediator derived from the omega-3 fatty acid, eicosapentaenoic acid, and has been shown to be involved in resolving inflammation. Although little is known about the actions of RvE1 in the resolution of inflammation due to asthma, recent studies in a mouse model have shown the possibilities of RvE1 in asthma. Objective/methods: We review the current understanding of the mechanism of RvE1 action in connection with asthma pathogenesis and treatment. Results/conclusion: Findings provide evidence for the use of RvE1 as a pivotal counter-regulatory signal in allergic inflammation and offer the possibility of novel multi-pronged therapeutic approaches for human asthma.