C16 Ceramide (d18:1/16:0)
(Synonyms: N-棕榈酰神经鞘氨醇,Palmitoyl Ceramide) 目录号 : GC43028
C16 神经酰胺(d18:1/16:0)是一种由神经酰胺合成酶 6(CerS6)生成的内源性神经酰胺,可作为脂质第二信使调控细胞凋亡和应激信号。C16 神经酰胺在诱导胰岛素抵抗中起着关键作用。.
Cas No.:24696-26-2
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >99.00%
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| Cell experiment [1]: | |
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Cell lines |
SW620 cells |
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Preparation Method |
Exogenous C16 ceramide sensitizes tumor cell to Fas-mediated apoptosis. SW620 cells were treated with C16 ceramide for 1 h at the indicated concentrations (0 - 3 µM ), and then cultured in the absence or presence of FasL for approximately 24 h. |
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Reaction Conditions |
0 - 3 µM; 24h |
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Applications |
Exogenous C16 ceramide directly induced apoptosis in a dose-dependent manner, albeit at a low level, exogenous C16 ceramide significantly increased SW620 cell sensitivity to FasL-induced apoptosis。 |
| Animal experiment [2]: | |
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Animal models |
Male C57BL/6J mice |
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Preparation Method |
Mice received repeated DH (the dorsal hippocampus) or BLA (the basolateral amygdala) infusions of vehicle, C8 ceramide ((d18:1/8:0); 2 µM/0.2 µL/side), C16 ceramide ((d18:1/16:0); 2 µM/0.2 µL/side), or C20 ceramide ((d18:1/20:0); 2 µM/0.2 µL/side). |
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Dosage form |
2 µM/0.2 µL/side; Intracerebral infusions. |
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Applications |
C16 ceramide induced a depressive-like phenotype when infused into the DH(the dorsal hippocampus), but a predominantly non-social anxiogenic-like phenotype when infused into the BLA(the basolateral amygdala). |
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References: [1] Paschall AV, et al. Ceramide targets xIAP and cIAP1 to sensitize metastatic colon and breast cancer cells to apoptosis induction to suppress tumor progression. BMC Cancer. 2014 Jan 15;14:24. | |
C16 ceramide (d18:1/16:0), as an endogenous ceramide, generated by ceramide synthase 6 (CerS6), that acts as a lipid second messenger to regulate apoptosis and stress signaling[1]. C16-ceramide plays a pivotal role in inducing insulin resistance[2].
In vitro, treatment with 100 µM synthetic C16 ceramide (d18:1/16:0), or accumulation of C16 ceramide (d18:1/16:0) through PPMP (30 µM) (namely, a selective inhibitor of glucosylceramide synthase) or MAPP (50 µM) (namely, a specific ceramidase inhibitor) induces apoptosis in neutrophil cultures via caspase-3 activation[3]. In vitro, 12 µM C16-ceramide treatment in HCT116 cells induces EMD (emerin) phosphorylation[4]. In vitro, 1 µM C16 ceramide partially rescued the LASP1-actin (play a role in cell migration) interaction under a CERS6 silencing condition[5]. Exogenous C16-ceramide (20 µM) and acid sphingomyelinase induced trophoblast apoptosis, an effect abrogated completely by cotreatment with 10 ng/ml EGF(epidermal growth factor)[6].
References:
[1]White-Gilbertson S, et al. Ceramide synthase 6 modulates TRAIL sensitivity and nuclear translocation of active caspase-3 in colon cancer cells. Oncogene. 2009 Feb 26;28(8):1132-41.
[2]Chathoth S, et al. Insulin resistance induced by de novo pathway-generated C16-ceramide is associated with type 2 diabetes in an obese population. Lipids Health Dis. 2022 Feb 20;21(1):24.
[3]Seumois G, et al. De novo C16- and C24-ceramide generation contributes to spontaneous neutrophil apoptosis. J Leukoc Biol. 2007 Jun;81(6):1477-86.
[4]Deroyer C, et al. New role for EMD (emerin), a key inner nuclear membrane protein, as an enhancer of autophagosome formation in the C16-ceramide autophagy pathway. Autophagy. 2014 Jul;10(7):1229-40.
[5]Payne SG, et al. Epidermal growth factor inhibits ceramide-induced apoptosis and lowers ceramide levels in primary placental trophoblasts. J Cell Physiol. 1999 Aug;180(2):263-70.
C16 神经酰胺(d18:1/16:0)是一种内源性神经酰胺,由神经酰胺合成酶 6(CerS6)生成,作为脂质第二信使调控细胞凋亡和应激信号[1]。C16 神经酰胺在诱导胰岛素抵抗中起着关键作用[2]。
在体外,用 100 µM 合成 C16 神经酰胺(d18:1/16:0)处理细胞,或通过 PPMP(30 µM)即一种葡萄糖甘油酰胺合成酶选择性抑制剂)或 MAPP(50 µM)(即一种特异性神经酰胺酶抑制剂) 积累的C16 神经酰胺(d18:1/16:0),可通过 caspase-3 激活诱导中性粒细胞凋亡[3]。在体外,用12 µM C16 神经酰胺处理 HCT116 细胞可诱导 EMD(emerin)磷酸化[4]。在体外,1 µM C16 神经酰胺可部分缓解 CERS6 沉默条件下 LASP1 与肌动蛋白(在细胞迁移中发挥作用)之间的相互作用[5]。外源性C16-神经酰胺(20 µM )和酸性鞘磷脂酶可诱导滋养细胞凋亡,与 10 毫微克/毫升 EGF(表皮生长因子)共处理可完全消除这种效应[6]。
| Cas No. | 24696-26-2 | SDF | |
| 别名 | N-棕榈酰神经鞘氨醇,Palmitoyl Ceramide | ||
| 化学名 | N-[(1S,2R,3E)-2-hydroxy-1-(hydroxymethyl)-3-heptadecen-1-yl]-hexadecanamide | ||
| Canonical SMILES | CCCCCCCCCCCCC/C=C/[C@@H](O)[C@@H](NC(CCCCCCCCCCCCCCC)=O)CO | ||
| 分子式 | C34H67NO3 | 分子量 | 537.9 |
| 溶解度 | DMF : 10 mg/mL (ultrasonic and warming and heat to 55°C) | 储存条件 | Store at -20°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 | 1.8591 mL | 9.2954 mL | 18.5908 mL |
| 5 mM | 0.3718 mL | 1.8591 mL | 3.7182 mL |
| 10 mM | 0.1859 mL | 0.9295 mL | 1.8591 mL |
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动物数量 | 只 |
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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.
Effect of Korean Red Ginseng on Plasma Ceramide Levels in Postmenopausal Women with Hypercholesterolemia: A Pilot Randomized Controlled Trial
Metabolites 2021 Jun 24;11(7):417.PMID:34202864DOI:10.3390/metabo11070417.
Cardiovascular disease (CVD) is a crucial cause of death in postmenopausal women. Plasma ceramide concentrations are correlated with the development of atherosclerosis and are significant predictors of CVD. Here, we conducted a 4-week, double-blinded, placebo-controlled clinical pilot study to investigate the effect of Korean red ginseng (KRG) on serum ceramide concentrations in 68 postmenopausal women with hypercholesterolemia. Patients were randomly assigned to two groups: the experimental group (n = 36) received KRG and the control (n = 32) group received placebo, 2 g each, once daily. Serum ceramides were measured using liquid chromatography-tandem mass spectrometry at baseline and study completion, with changes in serum ceramide levels as the primary end point. We detected significantly greater mean changes in C16 Ceramide levels (d18:1/16:0: -6.4 ± 6.3 pmol/mL vs. 14.6 ± 6.8 pmol/mL, respectively, p = 0.040; d18:1/22:0: -20.8 ± 24.4 pmol/mL vs. 71.1 ± 26.2 pmol/mL, respectively, p = 0.020). Additionally, changes in the median C16 (d18:1/16:0) and C22 (d18:1/22:0) ceramide levels were significantly greater in KRG-group subjects with metabolic syndrome than those without. Therefore, we found that KRG decreases the serum levels of several ceramides in postmenopausal women with hypercholesterolemia, suggesting it may be beneficial for preventing CVD in these individuals.
Activation of neutral sphingomyelinase 2 through hyperglycemia contributes to endothelial apoptosis via vesicle-bound intercellular transfer of ceramides
Cell Mol Life Sci 2021 Dec 24;79(1):48.PMID:34951654DOI:10.1007/s00018-021-04049-5.
Background: Pro-apoptotic and pro-inflammatory ceramides are crucially involved in atherosclerotic plaque development. Local cellular ceramide accumulation mediates endothelial apoptosis, especially in type 2 diabetes mellitus, which is a major cardiovascular risk factor. In recent years, large extracellular vesicles (lEVs) have been identified as an important means of intercellular communication and as regulators of cardiovascular health and disease. A potential role for lEVs as vehicles for ceramide transfer and inductors of diabetes-associated endothelial apoptosis has never been investigated. Methods and results: A mass-spectrometric analysis of human coronary artery endothelial cells (HCAECs) and their lEVs revealed C16 Ceramide (d18:1-16:0) to be the most abundant ceramide in lEVs and to be significantly increased in lEVs after hyperglycemic injury to HCAECs. The increased packaging of ceramide into lEVs after hyperglycemic injury was shown to be dependent on neutral sphingomyelinase 2 (nSMase2), which was upregulated in glucose-treated HCAECs. lEVs from hyperglycemic HCAECs induced apoptosis in the recipient HCAECs compared to native lEVs from untreated HCAECs. Similarly, lEVs from hyperglycemic mice after streptozotocin injection induced higher rates of apoptosis in murine endothelial cells compared to lEVs from normoglycemic mice. To generate lEVs with high levels of C16 Ceramide, ceramide was applied exogenously and shown to be effectively packaged into the lEVs, which then induced apoptosis in lEV-recipient HCAECs via activation of caspase 3. Intercellular transfer of ceramide through lEVs was confirmed by use of a fluorescently labeled ceramide analogue. Treatment of HCAECs with a pharmacological inhibitor of nSMases (GW4869) or siRNA-mediated downregulation of nSMase2 abrogated the glucose-mediated effect on apoptosis in lEV-recipient cells. In contrast, for small EVs (sEVs), hyperglycemic injury or GW4869 treatment had no effect on apoptosis induction in sEV-recipient cells. Conclusion: lEVs mediate the induction of apoptosis in endothelial cells in response to hyperglycemic injury through intercellular transfer of ceramides.
Long- and very long-chain ceramides are predictors of acute kidney injury in patients with acute coronary syndrome: the PEACP study
Cardiovasc Diabetol 2023 Apr 20;22(1):92.PMID:37081501DOI:10.1186/s12933-023-01831-6.
Background: Acute kidney injury (AKI) can be caused by multiple factors/events, including acute coronary syndrome (ACS). Ceramides are involved in atherosclerosis progression, cardiovascular events, and renal damage. Almost no studies have been conducted on the relationship between ceramide concentrations and AKI events. Therefore, we evaluated the association between plasma ceramide level at admission and AKI in patients with ACS undergoing percutaneous coronary intervention. Methods: We enrolled 842 ACS patients from the Prospective Multicenter Study for Early Evaluation of Acute Chest Pain. AKI was defined using the criteria from the 2012 Kidney Disease: Improving Global Outcomes. Eleven C16-C26 ceramides were measured using the high-performance liquid chromatography interfaced to tandem mass spectrometer procedure. Logistic regression models were used to evaluate relationships between ceramides and AKI risk. The area under the receiver operating characteristic curves (AUC) was used to evaluate differences between ceramides. Results: Overall, 139 (16.5%) patients developed AKI during hospitalisation. Patients who developed AKI had higher levels of Cer(d18:1/16:0), Cer(d18:1/18:0), Cer(d18:1/20:0), Cer(d18:1/21:0), Cer(d18:1/24:1), and Cer(d18:1/24:2) than patients who did not (P < 0.05). In risk-factor adjusted logistic regression models, these ceramides were independently associated with AKI risk (P < 0.05). Cer(d18:1/24:2) had the highest odds ratio of 3.503 (Q4 vs. Q1, 95% confidence interval: 1.743-7.040, P < 0.001). Ceramides had AUCs of 0.581-0.661 (P < 0.001) for AKI. Each ceramide combined with the Mehran risk score (AUC: 0.780) had AUCs of 0.802-0.808, greater than the Mehran risk score alone. Conclusion: Long-chain and very-long-chain ceramide levels may help determine the high AKI risk beyond traditional assessments.