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C16 Sphingomyelin (d18:1/16:0)

(Synonyms: N-棕榈酰-D-赤型鞘氨酰磷酸胆碱) 目录号 : GC43035

A sphingolipid

C16 Sphingomyelin (d18:1/16:0) Chemical Structure

Cas No.:6254-89-3

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1mg
¥960.00
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5mg
¥4,317.00
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10mg
¥7,675.00
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产品描述

Sphingomyelins are complex membrane lipids composed of phosphorylcholine, sphingosine, and an acylated group, such as a fatty acid. C16 Sphingomyelin is a form of sphingomyelin containing palmitate (16:0) at the variable acylation position. It is the most common form of sphingomyelin found in eggs and is less abundant in the brain and milk. C16 Sphingomyelin interacts with cholesterol in ordered lipid domains (lipid rafts). Sphingomyelinases remove phosphorylcholine from C16 sphingomyelin to produce C16 ceramide. While ceramides commonly induce apoptosis, ceramides with different fatty acid chain lengths might direct distinct functions and, in some cases, reduce apoptosis.

Chemical Properties

Cas No. 6254-89-3 SDF
别名 N-棕榈酰-D-赤型鞘氨酰磷酸胆碱
Canonical SMILES CCCCCCCCCCCCC/C=C/[C@@H](O)[C@@H](NC(CCCCCCCCCCCCCCCCC)=O)COP(OCC[N+](C)(C)C)([O-])=O
分子式 C39H79N2O6P 分子量 703
溶解度 Ethanol: 10 mg/ml 储存条件 Store at -20°C
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1 mM 1.4225 mL 7.1124 mL 14.2248 mL
5 mM 0.2845 mL 1.4225 mL 2.845 mL
10 mM 0.1422 mL 0.7112 mL 1.4225 mL
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Research Update

Phospholipids molecular species, proteins secondary structure, and emulsion microstructure of egg yolk with reduced polar and/or nonpolar lipids

Int J Biol Macromol 2023 Apr 1;233:123529.PMID:36740113DOI:10.1016/j.ijbiomac.2023.123529.

This study investigated the phospholipids (PLs) molecular species (PLs-MS), protein secondary structure (PSS), and emulsion microstructure of the egg yolk (EY) treated with supercritical-CO2 (T1), hexane (T2), and ethanol {at room temperature (T3) and 65 °C (T4)}. PLs-MS, PSS, and microstructure of EY emulsion were investigated with UPLC-Q-TOF-MS, Fourier-transforms infrared and Raman spectroscopy, and confocal laser scanning microscope, respectively. Predominant PLs molecular fractions were C18:0-C20:4, C18:0-C20:4, C16:0-C18:2, C16:0, C18:0-C18:2, and d18:1/16:0, for phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, lysophosphatidylcholine, sphingomyelin, and phosphatidylserine, respectively. All the PLs-MS were highest for T1 and many of them (C14:0-C16:0, C18:0-C18:1, C18:0-C20:3) were absent in T2, T3, and T4. PSS components (α-helices, β-sheets, β-turn, and random coil) were highest for T4, followed by T3, T2, T1, and control (non-treated EY). However, T1-added o/w emulsion showed excellent stability (95.64 %) with smaller and denser oil droplets due to better ionic interactions by synergistic effect of PLs-MS and PSS components.

CERTL reduces C16 ceramide, amyloid-β levels, and inflammation in a model of Alzheimer's disease

Alzheimers Res Ther 2021 Feb 17;13(1):45.PMID:33597019DOI:10.1186/s13195-021-00780-0.

Background: Dysregulation of ceramide and sphingomyelin levels have been suggested to contribute to the pathogenesis of Alzheimer's disease (AD). Ceramide transfer proteins (CERTs) are ceramide carriers which are crucial for ceramide and sphingomyelin balance in cells. Extracellular forms of CERTs co-localize with amyloid-β (Aβ) plaques in AD brains. To date, the significance of these observations for the pathophysiology of AD remains uncertain. Methods: A plasmid expressing CERTL, the long isoform of CERTs, was used to study the interaction of CERTL with amyloid precursor protein (APP) by co-immunoprecipitation and immunofluorescence in HEK cells. The recombinant CERTL protein was employed to study interaction of CERTL with amyloid-β (Aβ), Aβ aggregation process in presence of CERTL, and the resulting changes in Aβ toxicity in neuroblastoma cells. CERTL was overexpressed in neurons by adeno-associated virus (AAV) in a mouse model of familial AD (5xFAD). Ten weeks after transduction, animals were challenged with behavior tests for memory, anxiety, and locomotion. At week 12, brains were investigated for sphingolipid levels by mass spectrometry, plaques, and neuroinflammation by immunohistochemistry, gene expression, and/or immunoassay. Results: Here, we report that CERTL binds to APP, modifies Aβ aggregation, and reduces Aβ neurotoxicity in vitro. Furthermore, we show that intracortical injection of AAV, mediating the expression of CERTL, decreases levels of ceramide d18:1/16:0 and increases sphingomyelin levels in the brain of male 5xFAD mice. CERTL in vivo over-expression has a mild effect on animal locomotion, decreases Aβ formation, and modulates microglia by decreasing their pro-inflammatory phenotype. Conclusion: Our results demonstrate a crucial role of CERTL in regulating ceramide levels in the brain, in amyloid plaque formation and neuroinflammation, thereby opening research avenues for therapeutic targets of AD and other neurodegenerative diseases.