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Cell Research
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产品描述

Docosahexaenoic Acid (DHA) is an essential fatty acid and the most abundant ω-3 fatty acid in neural tissues, especially in the retina and brain. Docosahexaenoyl ethanolamide (DHEA) is the ethanolamine amide of DHA that has been detected in both brain and retina at concentrations similar to those for arachidonoyl ethanolamide (AEA).^1,2 A 9.5 fold increase of DHEA was observed in brain lipid extracts from piglets fed a diet supplemented with docosahexaenoic acid (DHA) compared to a control diet without DHA.³ DHEA binds to the rat brain CB₁ receptor with a K_i of 324 nM, which is approximately 10-fold higher than the K_i for AEA.⁴ DHEA inhibits shaker-related voltage-gated potassium channels in brain slightly better than AEA, with an IC₅₀ of 1.5 ?M.⁵

1.Sugiura, T., Kondo, S., Sukagawa, A., et al.Transacylase-mediated and phosphodiesterase-mediated synthesis of N-arachidonoylethanolamine, an endogenous cannabinoid-receptor ligand, in rat brain microsomes. Comparison with synthesis from free arachidonic acid and ethanolamineEur. J. Biochem.24053-62(1996) 2.Bisogno, T., Delton-Vandenbroucke, I., Milone, A., et al.Biosynthesis and inactivation of N-Arachidonoylethanolamine (Ananadamide) and N-Docosahexaenoylethanolamine in bovine retinaArch. Biochem. Biophys.370(2)300-307(1999) 3.Berger, A., Crozier, G., Bisogno, T., et al.Anandamide and diet: Inclusion of dietary arachidonate and docosahexaenoate leads to increased brain levels of the corresponding N-acylethanolamines in pigletsProc. Natl. Acad. Sci. USA98(11)6402-6406(2001) 4.Sheskin, T., Hanus, L., Slager, J., et al.Structural requirements for binding of anandamide-type compounds to the brain cannabinoid receptorJ. Med. Chem.40659-667(1997) 5.Poling, J.S., Rogawski, M.A., Salem, N., Jr., et al.Anadamide, an endogenous cannabinoid, inhibits shaker-related voltage-gated K+ channelsNeuropharmacology35(7)983-991(1996)

Chemical Properties

Cas No.	162758-94-3	SDF
别名	DEA, DHEA, Synaptamide
化学名	N-(2-hydroxyethyl)-4Z,7Z,10Z,13Z,16Z,19Z-docosahexaenamide
Canonical SMILES	CC/C=C\C/C=C\C/C=C\C/C=C\C/C=C\C/C=C\CCC(NCCO)=O
分子式	C₂₄H₃₇NO₂	分子量	371.56
溶解度	20mg/mL in DMSO or DMF	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。
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。

溶解性数据

制备储备液
		1 mg	5 mg	10 mg
	1 mM	2.6914 mL	13.4568 mL	26.9136 mL
	5 mM	0.5383 mL	2.6914 mL	5.3827 mL
	10 mM	0.2691 mL	1.3457 mL	2.6914 mL

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Research Update

N-Docosahexaenoylethanolamine ameliorates LPS-induced neuroinflammation via cAMP/PKA-dependent signaling

Background: Brain inflammation has been implicated as a critical mechanism responsible for the progression of neurodegeneration and characterized by glial cell activation accompanied by production of inflammation-related cytokines and chemokines. Growing evidence also suggests that metabolites derived from docosahexaenoic acid (DHA) have anti-inflammatory and pro-resolving effects; however, the possible role of N-docosahexaenoylethanolamine (synaptamide), an endogenous neurogenic and synaptogenic metabolite of DHA, in inflammation, is largely unknown. (The term "synaptamide" instead of "DHEA" was used for N-docosahexaenoylethanolamine since DHEA is a widely used and accepted term for the steroid, dehydroepiandrosterone.) In the present study, we tested this possibility using a lipopolysaccharide (LPS)-induced neuroinflammation model both in vitro and in vivo. Methods: For in vitro studies, we used P3 primary rat microglia and immortalized murine microglia cells (BV2) to assess synaptamide effects on LPS-induced cytokine/chemokine/iNOS (inducible nitric oxide synthase) expression by quantitative PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA). To evaluate in vivo effects, mice were intraperitoneally (i.p.) injected with LPS followed by synaptamide, and expression of proinflammatory mediators was measured by qPCR and western blot analysis. Activation of microglia and astrocyte in the brain was examined by Iba-1 and GFAP immunostaining. Results: Synaptamide significantly reduced LPS-induced production of TNF-α and NO in cultured microglia cells. Synaptamide increased intracellular cAMP levels, phosphorylation of PKA, and phosphorylation of CREB but suppressed LPS-induced nuclear translocation of NF-κB p65. Conversely, adenylyl cyclase or PKA inhibitors abolished the synaptamide effect on p65 translocation as well as TNF-α and iNOS expression. Administration of synaptamide following LPS injection (i.p.) significantly reduced neuroinflammatory responses, such as microglia activation and mRNA expression of inflammatory cytokines, chemokine, and iNOS in the brain. Conclusions: DHA-derived synaptamide is a potent suppressor of neuroinflammation in an LPS-induced model, by enhancing cAMP/PKA signaling and inhibiting NF-κB activation. The anti-inflammatory capability of synaptamide may provide a new therapeutic avenue to ameliorate the inflammation-associated neurodegenerative conditions.

Anandamide and other N-acylethanolamines: A class of signaling lipids with therapeutic opportunities

N-acylethanolamines (NAEs), including N-palmitoylethanolamine (PEA), N-oleoylethanolamine (OEA), N-arachidonoylethanolamine (AEA, anandamide), N-docosahexaenoylethanolamine (DHEA, synaptamide) and their oxygenated metabolites are a lipid messenger family with numerous functions in health and disease, including inflammation, anxiety and energy metabolism. The NAEs exert their signaling role through activation of various G protein-coupled receptors (cannabinoid CB₁ and CB₂ receptors, GPR55, GPR110, GPR119), ion channels (TRPV1) and nuclear receptors (PPAR-α and PPAR-γ) in the brain and periphery. The biological role of the oxygenated NAEs, such as prostamides, hydroxylated anandamide and DHEA derivatives, are less studied. Evidence is accumulating that NAEs and their oxidative metabolites may be aberrantly regulated or are associated with disease severity in obesity, metabolic syndrome, cancer, neuroinflammation and liver cirrhosis. Here, we comprehensively review NAE biosynthesis and degradation, their metabolism by lipoxygenases, cyclooxygenases and cytochrome P450s and the biological functions of these signaling lipids. We discuss the latest findings and therapeutic potential of modulating endogenous NAE levels by inhibition of their degradation, which is currently under clinical evaluation for neuropsychiatric disorders. We also highlight NAE biosynthesis inhibition as an emerging topic with therapeutic opportunities in endocannabinoid and NAE signaling.

Synaptamide (Dehydroepiandrosteron(DHEA))

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