Sinigrin
(Synonyms: 黑芥子苷) 目录号 : GC39138
Sinigrin是一种存在于十字花科植物中的具有口服活性的硫代葡萄糖苷。
Cas No.:3952-98-5
Sample solution is provided at 25 µL, 10mM.
Sinigrin is an orally active thioglucoside found in cruciferous plants[1]. Sinigrin exhibits diverse activities, including anticancer, antibacterial, antifungal, anti-inflammatory, antioxidant, and lipogenesis-inhibitory effects[2]. Sinigrin is commonly used in research on tumors, inflammatory, and metabolic diseases[3].
In vitro, Sinigrin (1-100μg/mL; 8 days) dose-dependently inhibits 3T3-L1 adipogenesis, activated AMPK/ACC and suppressing MAPK phosphorylation, and blocked lipid accumulation, PPARγ/C/EBPα expression, and pro-inflammatory cytokine release without cytotoxicity[4]. Sinigrin (20μM; 24-48h) exerts potent cytotoxicity against MCF-7 breast cancer cells, blocked PI3K/AKT/mTOR phosphorylation, triggered S-phase arrest, ROS overload, mitochondrial depolarization, and caspase-9-mediated apoptosis while suppressing cyclin D1, CDK4/6, PCNA and Bcl-2[5].
In vitro, Sinigrin (20mg/kg/d; 28 days; oral gavage) reversed MCAO-induced neuronal apoptosis, oxidative stress and neurological deficits while suppressing TLR4/MyD88 signaling in Sprague–Dawley rats[6]. Sinigrin (30mg/kg; 12 days; oral gavage) reversed DSS-induced colitis in BALB/c mice, suppressed IL-6, IL-1β, TNF-α and IL-17, restored antioxidant enzymes, and inhibited MAPK phosphorylation[7].
References:
[1] Awasthi S, Saraswathi NT. Sinigrin, a major glucosinolate from cruciferous vegetables restrains non-enzymatic glycation of albumin. Int J Biol Macromol. 2016;83:410-415.
[2] Melrose J. The Glucosinolates: A Sulphur Glucoside Family of Mustard Anti-Tumour and Antimicrobial Phytochemicals of Potential Therapeutic Application. Biomedicines. 2019;7(3):62.
[3] Mazumder A, Dwivedi A, du Plessis J. Sinigrin and Its Therapeutic Benefits. Molecules. 2016;21(4):416.
[4] Lee HW, Rhee DK, Kim BO, Pyo S. Inhibitory effect of sinigrin on adipocyte differentiation in 3T3-L1 cells: Involvement of AMPK and MAPK pathways. Biomed Pharmacother. 2018;102:670-680.
[5] Li S, Lin J, Wei J, Zhou L, Wang P. Sinigrin Impedes the Breast Cancer Cell Growth through the Inhibition of PI3K/AKT/mTOR Phosphorylation-Mediated Cell Cycle Arrest. J Environ Pathol Toxicol Oncol. 2022;41(3):33-43.
[6] Guo S, Lei Q, Yang Q, Chen R. Sinigrin improves cerebral ischaemia-reperfusion injury by inhibiting the TLR4 pathway-mediated oxidative stress. Chem Biol Drug Des. 2024;103(2):e14480.
[7] Kotipalli RSS, Tirunavalli SK, Pote AB, et al. Sinigrin Attenuates the Dextran Sulfate Sodium-induced Colitis in Mice by Modulating the MAPK Pathway. Inflammation. 2023;46(3):787-807.
Sinigrin是一种存在于十字花科植物中的具有口服活性的硫代葡萄糖苷[1]。Sinigrin具有抗癌、抗菌、抗真菌、抗炎、抗氧化及抑制脂肪生成等多种活性[2]。Sinigrin常用于肿瘤、炎症性及代谢性疾病的研究[3]。
体外实验中，Sinigrin（1-100μg/mL；作用8天）可剂量依赖性地抑制3T3-L1前脂肪细胞分化，激活AMPK/ACC通路并抑制MAPK磷酸化，阻断脂质积累及PPARγ/C/EBPα表达，减少促炎细胞因子释放，且无细胞毒性[4]。Sinigrin（20μM；24-48小时）对MCF-7乳腺癌细胞具有显著细胞毒性，可阻断PI3K/AKT/mTOR磷酸化，诱导S期阻滞、ROS过载、线粒体去极化及caspase-9介导的凋亡，并下调cyclin D1、CDK4/6、PCNA和Bcl-2[5]。
体内实验中，Sinigrin（20mg/kg/d；28天；灌胃）可逆转Sprague–Dawley大鼠MCAO模型中的神经元凋亡、氧化应激及神经功能缺损，并抑制TLR4/MyD88信号通路[6]。Sinigrin（30mg/kg；12天；灌胃）可逆转BALB/c小鼠DSS诱导的结肠炎，抑制IL-6、IL-1β、TNF-α和IL-17，恢复抗氧化酶水平，并抑制MAPK磷酸化[7]。
| Cell experiment [1]: | |
Cell lines | MCF-7 human breast cancer cells |
Preparation Method | MCF-7 human breast cancer cells were cultured in a humid environment with 5% CO2 (at 37°C) and kept aseptic conditions in a germ-free and fluid DMEM media with 100U/ml penicillin, 10% FBS, and 100μg/ml streptomycin. The MCF-7 cells attained the predicted confluency before being treated with Sinigrin (20μM) and were incubated in a CO2 incubator for 24 and 48 hours. The cells were extracted after incubation for future study. Sinigrin was dissolved in a molecular grade of 0.5% DMSO. MCF-7 cell viability was estimated through MTT analysis. The ROS and ΔΨm levels were investigated under the inverted fluorescence microscope. cell cycle was analysed by commercial kit according to instruction. Proteins were extracted for Western Blotting analysis. |
Reaction Conditions | 20μM; 24-48h |
Applications | Sinigrin exerts potent cytotoxicity against MCF-7 breast cancer cells, triggered S-phase arrest, ROS overload, mitochondrial depolarization, and caspase-9-mediated apoptosis while suppressing cyclin D1, CDK4/6, PCNA and Bcl-2. |
| Animal experiment [2]: | |
Animal models | Male adult Sprague-Dawley rats |
Preparation Method | Male Sprague–Dawley rats were provided with free access to food and water with a 12h light/dark cycle and environmental conditions of 22±2°C and approximately 60 humidity. The CIR model was established by middle cerebral artery occlusion (MCAO) surgery. The rats were randomly divided into four groups (n=10 per group): Sham, Sinigrin 20mg/mL, MCAO and MCAO+Sinigrin 20mg/kg. The rats in the Sham group underwent surgery without filament insertion. Rats in the Sinigrin 20mg/mL group received Sinigrin 20mg/kg/d via oral gavage for 28 days. The rats in the MCAO group underwent MCAO surgery. Rats in the MCAO+Sinigrin 20mg/kg groups received 20mg/kg/d sinigrin via oral gavage for 28days following MCAO surgery. At the end of the experiments, the rats were anaesthetised with 2% pentobarbital sodium and sacrificed to obtain the brain tissue. The tissues were fixed for H&E and TUNEL staining. Total proteins were extracted for Western Blotting analysis. The Neurological Deficit Score (NDS) was used to evaluate the neurological functional outcomes following Sinigrin treatment. |
Dosage form | 20mg/kg/d; 28 days; oral gavage |
Applications | Sinigrin reversed MCAO-induced neuronal apoptosis, oxidative stress and neurological deficits while suppressing TLR4/MyD88 signaling in Sprague–Dawley rats. |
References: | |
| Cas No. | 3952-98-5 | SDF | |
| 别名 | 黑芥子苷 | ||
| Canonical SMILES | O[C@@H]1[C@@H](O)[C@H](S/C(CC=C)=N/OS(=O)([O-])=O)O[C@H](CO)[C@H]1O.[K+] | ||
| 分子式 | C10H16KNO9S2 | 分子量 | 397.46 |
| 溶解度 | Water: 125 mg/mL (314.50 mM) | 储存条件 | Store at 2-8°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 | 2.516 mL | 12.5799 mL | 25.1598 mL |
| 5 mM | 503.2 μL | 2.516 mL | 5.032 mL |
| 10 mM | 251.6 μL | 1.258 mL | 2.516 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。
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Quality Control & SDS
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- Purity: >98.00%
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