Sodium ascorbate
(Synonyms: 维生素C钠; Sodium ascorbate; Sodium L-ascorbate; Vitamin C sodium salt) 目录号 : GC13616
Sodium ascorbate是一种内源性抗氧化剂，通过参与体内的羟化反应，促进细胞间质形成、辅助合成皮质激素，并通过促进叶酸还原和铁离子吸收来影响血细胞成熟，同时具有抗组胺和阻止亚硝胺生成的作用。
Cas No.:134-03-2
Sample solution is provided at 25 µL, 10mM.
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Sodium ascorbate is an endogenous antioxidant that participates in hydroxylation reactions in the body, promotes the formation of intercellular substances, assists in corticosteroid synthesis, and influences blood cell maturation by promoting folic acid reduction and iron ion absorption. Sodium ascorbate also possesses antihistaminic effects and inhibits the formation of nitrosamines[1-2]. Sodium ascorbate can be used for the prevention and treatment of scurvy, infectious diseases, acute attacks of Keshan disease, liver diseases, as well as adjuvant therapy for various anemias, allergic skin diseases, and cancer [3-4].
In vitro, Sodium ascorbate (10µM) treatment of B16 murine melanoma cells for 4 hours, Sodium ascorbate significantly induced apoptosis and downregulated transferrin receptor (TfR) expression, thereby reducing intracellular iron levels dependent on iron uptake[5]. Sodium ascorbate (0.5–3mM) treatment of human neuroblastoma cells (e.g., HTLA-230, SH-SY5Y) for 24 hours, Sodium ascorbate significantly induced caspase-dependent apoptosis, accompanied by loss of mitochondrial membrane potential, reduced cell proliferation, and decreased glycolytic capacity[6].
In vivo, Sodium ascorbate (60mg/kg) subcutaneously administered to tumor-bearing mice (P388 leukemia cells) (daily dosing starting from the first day after tumor implantation and continuing for 16 days), Sodium ascorbate significantly reduced tumor volume and weight, and improved mouse survival[7]. Sodium ascorbate (5mg/mouse) intraperitoneally administered to autoimmune arthritis mice (every other day for 21 days starting from the first day after immunization), Sodium ascorbate significantly delayed arthritis onset, reduced disease severity, and decreased autoantibody production[8].
References:
[1] Carr AC, Maggini S. Vitamin C and Immune Function. Nutrients. 2017 Nov 3;9(11):1211. doi: 10.3390/nu9111211.
[2] Padayatty SJ, Levine M. Vitamin C: the known and the unknown and Goldilocks. Oral Dis. 2016 Sep;22(6):463-93.
[3] Gęgotek A, Skrzydlewska E. Ascorbic acid as antioxidant. Vitam Horm. 2023;121:247-270.
[4] Moores J. Vitamin C: a wound healing perspective. Br J Community Nurs. 2013 Dec;Suppl:S6, S8-11.
[5] Kang JS, Cho D, Kim YI, et al. Sodium ascorbate (vitamin C) induces apoptosis in melanoma cells via the down-regulation of transferrin receptor dependent iron uptake. J Cell Physiol. 2005 Jul;204(1):192-7.
[6] Carosio R, Zuccari G, Orienti I, et al. Sodium ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake. Mol Cancer. 2007 Aug 30;6:55.
[7] Osswald H, Herrmann R, Youssef M. The influence of sodium ascorbate, menadione sodium bisulfite or pyridoxal hydrochloride on the toxic and antineoplastic action of N-methylformamide in P 388 leukemia or M 5076 sarcoma in mice. Toxicology. 1987 Feb;43(2):183-91.
[8] Yin Y, Wu S. Ascorbic acid alleviates rheumatoid arthritis by inhibiting the production of autoantibodies. Cell Commun Signal. 2024 Jul 24;22(1):373.
Sodium ascorbate是一种内源性抗氧化剂，通过参与体内的羟化反应，促进细胞间质形成、辅助合成皮质激素，并通过促进叶酸还原和铁离子吸收来影响血细胞成熟，同时具有抗组胺和阻止亚硝胺生成的作用[1-2]。Sodium ascorbate可用于防治坏血病、感染性疾病、克山病急性发作、肝脏疾病，以及多种贫血、过敏性皮肤病和癌症的辅助治疗[3-4]。
在体外，Sodium ascorbate（10μM）处理B16鼠源黑色素瘤细胞4小时，可显著诱导细胞凋亡，并下调转铁蛋白受体（TfR）表达，从而减少铁摄取依赖的细胞内铁水平[5]。Sodium ascorbate（0.5–3mM）处理人源神经母细胞瘤细胞（如HTLA-230、SH-SY5Y）24小时，可显著诱导caspase依赖性凋亡，并伴随线粒体膜电位丧失、细胞增殖与糖酵解能力降低[6]。
在体内，Sodium ascorbate（60mg/kg）皮下注射处理荷瘤（P388白血病细胞）小鼠（每日给药，从肿瘤植入后第1天开始持续16天），Sodium ascorbate显著降低肿瘤形成的体积和重量，提高小鼠生存期 [7]。Sodium ascorbate（5mg/只）腹腔注射处理自身免疫性关节炎小鼠（隔日一次，从免疫后第1天持续21天），Sodium ascorbate显著延迟关节炎发病时间、降低疾病严重程度，并减少自身抗体的产生[8]。
| Cell experiment [1]: | |
Cell lines | Human neuroblastoma cell lines (HTLA-230, IMR-32, LAN-5, GI-LI-N, SH-SY5Y) |
Preparation Method | Cells were maintained in Dulbecco’s modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum (FBS), 2mM L-glutamine, and antibiotics at 37°C, 5% CO₂. Cells were treated with Sodium Ascorbate at concentrations ranging from 0.5mM to 3mM for 6–24 hours. |
Reaction Conditions | 0.5–3mM; 6–24h |
Applications | Sodium Ascorbate induced dose- and time-dependent apoptosis in all neuroblastoma cell lines, characterized by an increase in sub-G1 phase cells and caspase activation. Sodium Ascorbate significantly downregulated transferrin receptor (TfR/CD71) expression, leading to reduced intracellular iron levels. Treatment with Sodium Ascorbate also caused early loss of mitochondrial membrane potential (ΔΨm), and these effects were reversible by the iron donor ferric ammonium citrate (FAC), confirming iron depletion as the key mechanism of apoptosis. |
| Animal experiment [2]: | |
Animal models | C57BL/6 mice with collagen-induced arthritis (CIA) or lupus-like autoimmune disease (bm12-induced model) |
Preparation Method | Mice were intraperitoneally injected with Sodium Ascorbate (5mg/mouse, dissolved in PBS) every other day for 7–21 days. For CIA, immunization with chicken type II collagen (CII) was performed 1 day after the first Sodium Ascorbate injection. For antibody response studies, mice were immunized with NP-Ficoll (T-independent) or NP-KLH (T-dependent) antigens. |
Dosage form | 5mg/mouse; i.p.; intermittent injection (every 48h). |
Applications | Sodium Ascorbate significantly delayed arthritis onset and reduced disease severity in CIA mice, as evidenced by decreased clinical scores, synovial inflammation, cartilage/bone damage, and osteoclast activity. Sodium Ascorbate also suppressed autoantibody production (e.g., collagen-specific IgG and rheumatoid factor) in both arthritis and lupus models. Mechanistically, ascorbic acid inhibited B cell differentiation into plasma cells, disrupted germinal center formation, and impaired antibody affinity maturation by blocking STAT3 signaling and promoting B cell apoptosis. |
References: | |
| Cas No. | 134-03-2 | SDF | |
| 别名 | 维生素C钠; Sodium ascorbate; Sodium L-ascorbate; Vitamin C sodium salt | ||
| 化学名 | sodium (R)-2-((S)-1,2-dihydroxyethyl)-4-hydroxy-5-oxo-2,5-dihydrofuran-3-olate | ||
| Canonical SMILES | O=C1C(O)=C([O-])[C@@H]([C@@H](O)CO)O1.[Na+] | ||
| 分子式 | C6H7NaO6 | 分子量 | 198.11 |
| 溶解度 | ≥ 9.1mg/mL in Water | 储存条件 | 4°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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.0477 mL | 25.2385 mL | 50.477 mL |
| 5 mM | 1.0095 mL | 5.0477 mL | 10.0954 mL |
| 10 mM | 504.8 μL | 2.5239 mL | 5.0477 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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2.
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