Resolvin D3
(Synonyms: RvD3) 目录号 : GC44817A DHA-derived trihydroxy resolvin
Cas No.:916888-47-6
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
Resolvins are a family of potent lipid mediators derived from both eicosapentaenoic acid and docosahexaenoic acid . [1] In addition to being anti-inflammatory, resolvins promote the resolution of the inflammatory response. [2] Resolvin D3 (RvD3) is a DHA-derived product first identified in mouse inflammatory exudates.[3] It reduces neutrophil infiltration in vivo in both mouse peritonitis and dermal inflammation. [3] In addition to suppressing leukocyte migration, RvD3 enhances macrophage phagocytosis and efferocytosis [4]. Unlike other resolvins, RvD3 appears late in resolution in mouse peritonitis. [4] [5] Analytical and biological comparisons of synthetic RvD3 with endogenously derived RvD3 have confirmed its identity as matching the natural product. [6]
Reference：
[1]. Hong, S., Gronert, K., Devchand, P.R., et al. Novel docosatrienes and 17S-resolvins generated from docosahexaenoic acid in murine brain, human blood, and glial cells. Autacoids in anti-inflammation. J. Biol. Chem. 278(17), 14677-14687 (2003).
[2]. Ariel, A., and Serhan, C.N. Resolvins and protectins in the termination program of acute inflammation. TRENDS in Immunology 28(4), 176-183 (2007).
[3]. 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).
[4]. Dalli, J., Winkler, J.W., Colas, R.A., et al. Resolvin D3 and aspirin-triggered resolvin D3 are potent immunoresolvents. Chem. Biol. 20(2), 188-201 (2015).
[5]. Serhan, C.N. Novel pro-resolving lipid mediators in inflammation are leads for resolution physiology. Nature 510(7503), 92-101 (2014).
[6]. Serhan, C. . (2007).
| Cas No. | 916888-47-6 | SDF | |
| 别名 | RvD3 | ||
| 化学名 | 4S,11R,17S-trihydroxy-5Z,7E,9E,13Z,15E,19Z-docosahexaenoic acid | ||
| Canonical SMILES | O[C@@H](CCC(O)=O)/C=C\C=C\C=C\[C@H](O)C/C=C\C=C\[C@@H](O)C/C=C\CC | ||
| 分子式 | C22H32O5 | 分子量 | 376.5 |
| 溶解度 | 50 mg/ml in DMF, 50 mg/ml 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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| 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 | 2.656 mL | 13.2802 mL | 26.5604 mL |
| 5 mM | 0.5312 mL | 2.656 mL | 5.3121 mL |
| 10 mM | 0.2656 mL | 1.328 mL | 2.656 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 D3 controls mouse and human TRPV1-positive neurons and preclinical progression of psoriasis
Theranostics 2020 Oct 26;10(26):12111-12126.PMID:33204332DOI:10.7150/thno.52135.
Rationale: Psoriasis is a chronic inflammatory disease caused by a complex interplay between the immune and nervous systems with recurrent scaly skin plaques, thickened stratum corneum, infiltration and activation of inflammatory cells, and itch. Despite an increasing availability of immune therapies, they often have adverse effects, high costs, and dissociated effects on inflammation and itch. Activation of sensory neurons innervating the skin and TRPV1 (transient receptor potential vanilloid 1) are emerging as critical components in the pathogenesis of psoriasis, but little is known about their endogenous inhibitors. Recent studies have demonstrated that resolvins, endogenous lipid mediators derived from omega-3 fatty acids, are potent inhibitors of TRP channels and may offer new therapies for psoriasis without known adverse effects. Methods: We used behavioral, electrophysiological and biochemical approaches to investigate the therapeutic effects of Resolvin D3 (RvD3), a novel family member of resolvins, in a preclinical model of psoriasis consisting of repeated topical applications of imiquimod (IMQ) to murine skin, which provokes inflammatory lesions that resemble human psoriasis. Results: We report that RvD3 specifically reduced TRPV1-dependent acute pain and itch in mice. Mechanistically, RvD3 inhibited capsaicin-induced TRPV1 currents in dissociated dorsal root ganglion (DRG) neurons via the N-formyl peptide receptor 2 (i.e. ALX/FPR2), a G-protein coupled receptor. Single systemic administration of RvD3 (2.8 mg/kg) reversed itch after IMQ, and repeated administration largely prevented the development of both psoriasiform itch and skin inflammation with concomitant decreased in calcitonin gene-related peptide (CGRP) expression in DRG neurons. Accordingly, specific knockdown of CGRP in DRG was sufficient to prevent both psoriasiform itch and skin inflammation similar to the effects following RvD3 administration. Finally, we elevated the translational potential of this study by showing that RvD3 significantly inhibited capsaicin-induced TRPV1 activity and CGRP release in human DRG neurons. Conclusions: Our findings demonstrate a novel role for RvD3 in regulating TRPV1/CGRP in mouse and human DRG neurons and identify RvD3 and its neuronal pathways as novel therapeutic targets to treat psoriasis.
Total synthesis of Resolvin D3
Org Biomol Chem 2022 Jun 1;20(21):4338-4341.PMID:35551327DOI:10.1039/d2ob00750a.
Resolvin D3 was synthesized by the Suzuki-Miyaura cross-coupling reaction of C1-C8 borane with C9-C22 iodoolefin as the key reaction. The latter intermediate was obtained by the sequential Wittig reactions of C9-C13 phosphonium salt with C14-C19 aldehyde and then C9-C19 aldehyde with propyltriphenylphosphonium bromide. The stereogenic centers at C4, C11, and C17 were constructed by the ruthenium-catalyzed asymmetric transfer hydrogenation with high stereoselectivity.
Resolvin D3 Promotes Inflammatory Resolution, Neuroprotection, and Functional Recovery After Spinal Cord Injury
Mol Neurobiol 2021 Jan;58(1):424-438.PMID:32964315DOI:10.1007/s12035-020-02118-7.
Resolvins, a new family from the endogenous specialized pro-resolving mediators (SPMs), promote the resolution of the inflammatory response. Resolvin D3 (RvD3), a docosahexaenoic acid (DHA) product, has been known to suppress the inflammatory response. However, the anti-inflammatory and neuroprotective effects of RvD3 are not known in a model of spinal cord injury (SCI). Here, we investigated the anti-inflammatory and neuroprotective effect of RvD3 in a mouse model of SCI. Processes associated with anti-inflammation and angiogenesis were studied in RAW 264.7 cells and the human brain endothelial cell line hCMEC/D3, respectively. Additionally, female C57BL/6 mice were subjected to moderate compression SCI (20-g weight compression for 1 min) followed by intrathecal injection of vehicle or RvD3 (1 μg/20 μL) at 1 h post-SCI. RvD3 decreased the lipopolysaccharide (LPS)-induced production of inflammatory mediators and nitric oxide (NO) in RAW 264.7 cells and promoted an angiogenic effect in the hCMEC/D3 cell line. Treatment with RvD3 improved locomotor recovery and reduced thermal hyperalgesia in SCI mice compared with vehicle treatment at 14 days post-SCI. Remarkably, RvD3-treated mice exhibited reduced expression of inflammatory cytokines (TNF-α, IL6, IL1β) and chemokines (CCL2, CCL3). Also, RvD3-treated mice exhibited increased expression of tight junction proteins such as zonula occludens (ZO)-1 and occludin. Furthermore, immunohistochemistry showed a decreased level of gliosis (GFAP, Iba-1) and neuroinflammation (CD68, TGF-β) and enhanced neuroprotection. These data provide evidence that intrathecal injection of RvD3 represents a promising therapeutic strategy to promote inflammatory resolution, neuroprotection, and neurological functional recovery following SCI.
Resolvin D3 improves the impairment of insulin signaling in skeletal muscle and nonalcoholic fatty liver disease through AMPK/autophagy-associated attenuation of ER stress
Biochem Pharmacol 2022 Sep;203:115203.PMID:35948170DOI:10.1016/j.bcp.2022.115203.
Resolvin D3 (RD3), an endogenous lipid mediator derived from omega-3 fatty acids, has been documented to attenuate inflammation in various disease models. Although it has been reported that omega-3 fatty acids attenuate metabolic disorders, the roles of RD3 in insulin signaling in skeletal muscle and hepatic lipid metabolism remain unclear. In the current study, we examined the role of RD3 in skeletal muscle insulin resistance and hepatic steatosis using in vitro and in vivo obesity models. In mouse primary hepatocytes, RD3 treatment reduced lipid accumulation and the production of lipogenic proteins (processed SREBP1 and SCD1) while improving insulin signaling in C2C12 myocytes. Furthermore, RD3 treatment ameliorated palmitate-induced ER stress markers (phospho-eIF2α and CHOP) in mouse primary hepatocytes and C2C12 myocytes. Treatment with RD3 increased phospho-AMPK expression and autophagy markers (LC3 conversion, p62 degradation, and autophagosome formation). AMPK siRNA or 3-MA reduced the effects of RD3 on C2C12 myocytes and mouse primary hepatocytes treated with palmitate. Finally, we confirmed the therapeutic effects of RD3 on skeletal muscle insulin resistance and hepatic lipid metabolism in high-fat diet (HFD)-fed mice. In vivo transfection-mediated suppression of AMPK restored all these changes in animal models. The results of the present study suggest that RD3 alleviates insulin resistance in skeletal muscle and hepatic steatosis via AMPK/autophagy signaling and provides an effective and safe therapeutic approach for treating metabolic disorders, including insulin resistance, type 2 diabetes, and NAFLD.
Human leukocytes selectively convert 4 S,5 S-epoxy-resolvin to Resolvin D3, resolvin D4, and a cys-resolvin isomer
Proc Natl Acad Sci U S A 2021 Dec 21;118(51):e2116559118.PMID:34911767DOI:10.1073/pnas.2116559118.
Human phagocytes have key functions in the resolution of inflammation. Here, we assessed the role of the proposed 4S,5S-epoxy-resolvin intermediate in the biosynthesis of both Resolvin D3 and resolvin D4. We found that human neutrophils converted this synthetic intermediate to Resolvin D3 and resolvin D4. M2 macrophages transformed this labile epoxide intermediate to resolvin D4 and a previously unknown cysteinyl-resolvin isomer without appreciable amounts of Resolvin D3. M2 macrophages play critical roles in the resolution of inflammation and in wound healing. Human M2 macrophages also converted leukotriene A4 to lipoxins. The cysteinyl-resolvin isomer significantly accelerated tissue regeneration of surgically injured planaria. In a model of human granuloma formation, the cysteinyl-resolvin isomer significantly inhibited granuloma development by human peripheral blood leukocytes. Together, these results provide evidence for a human cell type-specific role of 4S,5S-epoxy-resolvin in the biosynthesis of Resolvin D3 by neutrophils, resolvin D4 by both M2 macrophages and neutrophils, and a unique cysteinyl-resolvin isomer produced by M2 macrophages that carries potent biological activities in granuloma formation and tissue regeneration.