N-Acetylneuraminic acid是一种天然存在于结肠中的唾液酸。N-Acetylneuraminic acid作为细胞表面糖蛋白和糖脂的关键组成成分，参与细胞识别、信号传导与黏附。
Cas No.:131-48-6
Sample solution is provided at 25 µL, 10mM.
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N-Acetylneuraminic acid is a sialic acid naturally present in the colon. As a key component of cell surface glycoproteins and glycolipids, N-Acetylneuraminic acid participates in cell recognition, signal transduction, and adhesion. N-Acetylneuraminic acid can bind to pathogens, preventing their adhesion and invasion of host cells, thereby exerting antiviral and antibacterial effects, while enhancing immune function by regulating immune cell activity. N-Acetylneuraminic acid can be used in infant formula, functional foods and health products, as well as in research related to anti-influenza drugs and coronary heart disease[1-4].
In vitro, After 8 hours of hypoxia and glucose deprivation, H9C2 cardiomyocytes were treated with N-Acetylneuraminic acid (30mM) for 3 hours under reoxygenation conditions. N-Acetylneuraminic acid significantly increased superoxide dismutase (SOD) activity, elevated intracellular Fe²⁺ and lipid peroxide levels, reduced the protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2), glutathione peroxidase 4 (GPX4), cystine/glutamate antiporter (xCT), heme oxygenase-1 (HO-1), and ferroptosis suppressor protein 1 (FSP1), and promoted ferroptosis in cardiomyocytes[5]. N-Acetylneuraminic acid (20mM) was used to treat HUVECs for 24 hours. N-Acetylneuraminic acid significantly inhibited cell viability and increased the apoptosis rate, upregulated the protein and mRNA expression of inflammatory markers ICAM-1 and IL-1β, and decreased the levels of autophagy-related proteins LC3 II and SQSTM1/p62[6].
In vivo, N-Acetylneuraminic acid (500mg/kg) was subcutaneously injected twice daily into 5xFAD mice for 7 days. N-Acetylneuraminic acid replicated the effects of a high-fat diet on CD4⁺ T cells and accelerated recognition memory impairment[7]. N-Acetylneuraminic acid (60mg/kg/day) was intraperitoneally injected into high-fat diet-induced ApoE⁻/⁻ mice for five consecutive weeks. N-Acetylneuraminic acid significantly aggravated atherosclerotic lesions in mice, including increased lipid deposition, enlarged plaque necrotic core area, enhanced expression of pro-inflammatory cytokines and oxidative stress, and drove macrophage polarization toward a pro-inflammatory M1 phenotype[8].
References:
[1] Zhang L, Wei TT, Li Y, et al. Functional Metabolomics Characterizes a Key Role for N-Acetylneuraminic Acid in Coronary Artery Diseases. Circulation. 2018 Mar 27;137(13):1374-1390.
[2] Yida Z, Imam MU, Ismail M, et al. High fat diet-induced inflammation and oxidative stress are attenuated by N-acetylneuraminic acid in rats. J Biomed Sci. 2015 Oct 24;22:96.
[3] Kiefel MJ, Beisner B, Bennett S, et al. Synthesis and biological evaluation of N-acetylneuraminic acid-based rotavirus inhibitors. J Med Chem. 1996 Mar 15;39(6):1314-20.
[4] Bian D, Wang X, Huang J, et al. Maternal Neu5Ac Supplementation During Pregnancy Improves Offspring Learning and Memory Ability in Rats. Front Nutr. 2021 Oct 13;8:641027.
[5] Ji C, Zuo Z, Wang J, et al. N-acetylneuraminic acid promotes ferroptosis of H9C2 cardiomyocytes with hypoxia/reoxygenation injury by inhibiting the Nrf2 axis. Nan Fang Yi Ke Da Xue Xue Bao. 2025 Jan 20;45(1):72-79.
[6] Chen L, Qiu H, Chen Q, et al. N-acetylneuraminic acid modulates SQSTM1/p62 sialyation-mediated ubiquitination degradation contributing to vascular endothelium dysfunction in experimental atherosclerosis mice. IUBMB Life. 2024 Mar;76(3):161-178.
[7] Suzzi S, Croese T, Ravid A, et al. N-acetylneuraminic acid links immune exhaustion and accelerated memory deficit in diet-induced obese Alzheimer's disease mouse model. Nat Commun. 2023 Mar 9;14(1):1293.
[8] Huang D, Yin C, Wang D. Neu5Ac promotes high-fat diet-induced progression of atherosclerosis in Apoe-deficient mice. Exp Anim. 2025 Dec 3.
N-Acetylneuraminic acid是一种天然存在于结肠中的唾液酸。N-Acetylneuraminic acid作为细胞表面糖蛋白和糖脂的关键组成成分，参与细胞识别、信号传导与黏附。N-Acetylneuraminic acid能够与病原体结合阻止其黏附和入侵宿主细胞，从而发挥抗病毒和抗菌作用，同时通过调节免疫细胞活性增强机体免疫功能。N-Acetylneuraminic acid可用于婴幼儿配方食品、功能性食品与保健品，以及抗流感药物和冠心病相关研究[1-4]。
在体外，缺氧缺糖8h后，在复氧的条件下，N-Acetylneuraminic acid（30mM）处理H9C2心肌细胞3h。N-Acetylneuraminic acid显著提高超氧化物歧化酶（SOD）活性，增加细胞内Fe²⁺和脂质过氧化物水平，降低核因子E2相关因子2（Nrf2）、谷胱甘肽过氧化物酶4（GPX4）、胱氨酸/谷氨酸反向转运体（xCT）、血红素加氧酶-1（HO-1）和铁死亡抑制蛋白1（FSP1）蛋白的表达，并促进心肌细胞发生铁死亡[5]。N-Acetylneuraminic acid（20mM）处理HUVECs细胞24小时。N-Acetylneuraminic acid显著抑制细胞活力并增加细胞凋亡率，同时上调炎症标志物ICAM-1和IL-1β的蛋白及mRNA表达，并降低自噬相关蛋白LC3 II和SQSTM1/p62的水平[6]。
在体内，N-Acetylneuraminic acid（500mg/kg）每天两次皮下注射于5xFAD小鼠，持续7天。N-Acetylneuraminic acid重现了高脂饮食对CD4+ T细胞的影响并加速了识别记忆障碍[7]。N-Acetylneuraminic acid（60mg/kg/day）腹腔注射于高脂饮食诱导的ApoE-/-小鼠，连续五周。N-Acetylneuraminic acid显著加重了小鼠动脉粥样硬化病变，增加脂质沉积、扩大斑块坏死核心面积、增强促炎细胞因子表达和氧化应激，并驱动巨噬细胞向促炎M1表型极化[8]。
| Cell experiment [1]: | |
Cell lines | HUVECs (Human Umbilical Vein Endothelial Cells) |
Preparation Method | HUVECs were cultured in DMEM medium supplemented with 10% fetal bovine serum and 1% antibiotics (penicillin/streptomycin) at 37°C, 5% CO₂. Cells were treated with N-Acetylneuraminic acid (20mM). |
Reaction Conditions | 20mM; 24h |
Applications | N-Acetylneuraminic acid significantly inhibited cell viability and increased apoptosis rate in a dose-dependent manner. N-Acetylneuraminic acid upregulated the protein and mRNA expression of inflammation markers ICAM-1 and IL-1β. N-Acetylneuraminic acid decreased the levels of autophagy-related proteins LC3 II and SQSTM1/p62. |
| Animal experiment [2]: | |
Animal models | ApoE-/- mice (C57BL/6J background) |
Preparation Method | Mice were fed a high-fat diet to induce atherosclerosis. N-Acetylneuraminic acid (60mg/kg/day) was administered via intraperitoneal injection once daily for five consecutive weeks. |
Dosage form | 60mg/kg/day; i.p.; once daily for five consecutive weeks |
Applications | N-Acetylneuraminic acid significantly aggravated atherosclerotic lesions, including increased lipid deposition, enlarged plaque necrotic core area, enhanced expression of pro-inflammatory cytokines (TNF-α, IL-6, MCP-1), elevated oxidative stress, and drove macrophage polarization towards a pro-inflammatory M1 phenotype. |
References: | |
| Cas No. | 131-48-6 | SDF | |
| 别名 | 唾液酸; NANA; Lactaminic acid | ||
| 化学名 | (2S,4S,5R,6R)-2,4-dihydroxy-5-((Z)-(1-hydroxyethylidene)amino)-6-((1R,2R)-1,2,3-trihydroxypropyl)tetrahydro-2H-pyran-2-carboxylic acid | ||
| Canonical SMILES | C/C(O)=N/[C@]([C@](O1)([H])[C@@](O)([H])[C@@](O)([H])CO)([H])[C@](O)([H])C[C@@]1(O)C(O)=O | ||
| 分子式 | C11H19NO9 | 分子量 | 309.27 |
| 溶解度 | ≥ 30.9mg/mL in Water | 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 | 3.2334 mL | 16.1671 mL | 32.3342 mL |
| 5 mM | 646.7 μL | 3.2334 mL | 6.4668 mL |
| 10 mM | 323.3 μL | 1.6167 mL | 3.2334 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。
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