Sinigrin
(Synonyms: 黑芥子苷) 目录号 : GC39138
A glucosinolate with diverse biological activities
Cas No.:3952-98-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Sinigrin is a glucosinolate that has been found in Brassica and has diverse biological activities.1,2,3 It inhibits NOD-like receptor protein 3 (NLRP3) inflammasome activation in ATP-stimulated, LPS-primed RAW 264.7 cells in a concentration-dependent manner.1 Sinigrin (1-100 ?g/ml) reduces LPS-induced production of nitric oxide (NO) and prostaglandin E2 , as well as NF-κB activation, in RAW 264.7 cells. It induces cell cycle arrest at the G0/G1 phase in HepG2 hepatocellular carcinoma cells when used at concentrations of 0.1 and 0.5 mM.2 Sinigrin (10 and 20 mg/kg) reduces increases in renal glomerular basement membrane thickness, as well as increases in systolic and diastolic blood pressure, in a rat model of hypertension induced by angiotensin II.3
1.Lee, H.-W., Lee, C.G., Rhee, D.-K., et al.Sinigrin inhibits production of inflammatory mediators by suppressing NF-κB/MAPK pathways or NLRP3 inflammasome activation in macrophagesInt. Immunopharmacol.45163-173(2017) 2.Jie, M., Cheung, W.M., Yu, V., et al.Anti-proliferative activities of sinigrin on carcinogen-induced hepatotoxicity in ratsPLoS One9(10)e110145(2014) 3.Cong, C., Yuan, X., Hu, Y., et al.Sinigrin attenuates angiotensin II?induced kidney injury by inactivating nuclear factor?κB and extracellular signal?regulated kinase signaling in vivo and in vitroInt. J. Mol. Med.48(2)161(2021)
| 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 | 0.5032 mL | 2.516 mL | 5.032 mL |
| 10 mM | 0.2516 mL | 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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Sinigrin and Its Therapeutic Benefits
Molecules 2016 Mar 29;21(4):416.PMID:27043505DOI:10.3390/molecules21040416.
Sinigrin (allyl-glucosinolate or 2-propenyl-glucosinolate) is a natural aliphatic glucosinolate present in plants of the Brassicaceae family, such as broccoli and brussels sprouts, and the seeds of Brassica nigra (mustard seeds) which contain high amounts of Sinigrin. Since ancient times, mustard has been used by mankind for its culinary, as well as medicinal, properties. It has been systematically described and evaluated in the classical Ayurvedic texts. Studies conducted on the pharmacological activities of Sinigrin have revealed anti-cancer, antibacterial, antifungal, antioxidant, anti-inflammatory, wound healing properties and biofumigation. This current review will bring concise information about the known therapeutic activities of Sinigrin. However, the information on known biological activities is very limited and, hence, further studies still need to be conducted and its molecular mechanisms also need to be explored. This review on the therapeutic benefits of Sinigrin can summarize current knowledge about this unique phytocompounds.
Sinigrin attenuates angiotensin II‑induced kidney injury by inactivating nuclear factor‑κB and extracellular signal‑regulated kinase signaling in vivo and in vitro
Int J Mol Med 2021 Aug;48(2):161.PMID:34278443DOI:10.3892/ijmm.2021.4994.
The present study investigated the function of Sinigrin in angiotensin II (Ang II)‑induced renal damage. The results demonstrated that systolic blood pressure (SBP) and diastolic blood pressure (DBP) were increased in Ang II‑challenged rats, and Sinigrin treatment inhibited their increase. The levels of blood urea nitrogen (BUN) and serum creatinine (SCR) were increased by Ang II in the rats, and these were reversed by Sinigrin in a dose‑dependent manner. In addition, the Ang II‑induced elevation of urinary protein levels was inhibited by Sinigrin treatment. Glomerular basement membrane thickness and ECM degradation markers, such as collagen I, collagen IV and fibronectin, were suppressed by Sinigrin in the Ang II‑challenged rats. Moreover, the levels of inflammatory regulators, including tumor necrosis factor‑α (TNF‑α), interleukin‑6 (IL‑6) and monocyte chemoattractant protein‑1 (MCP‑1), were reduced following Sinigrin treatment of the Ang II‑challenged rats and in Ang II‑exposed proximal tubule epithelial cells. Furthermore, the superoxide dismutase (SOD) and catalase (CAT) levels were downregulated, whereas the malondialdehyde (MDA) levels were upregulated by Ang II; these effects were reversed by Sinigrin treatment in vivo and in vitro. Mechanistically, Sinigrin inhibited the Ang II‑induced phosphorylation of ERK, p65 and IκBα. Thus, Sinigrin attenuated Ang II‑induced renal injury by inactivating ERK and NF‑κB signaling. Sinigrin may thus prove to be a potential candidate for the treatment of hypertension‑induced kidney damage.
Antidiabetic Potential of Sinigrin Against Streptozotocin-Induced Diabetes via Modulating Inflammation and Oxidative Stress
Appl Biochem Biotechnol 2022 Oct;194(10):4279-4291.PMID:34780044DOI:10.1007/s12010-021-03739-x.
Diabetes mellitus (DM) is a common metabolic disorder which arises due to the improper carbohydrate metabolism, decreased secretion/activity of insulin, and genetic abnormalities, which result in the increased blood glucose level generally known as hyperglycemia. Diabetes holds an increased global prevalence in each year and is responsible for increased morbidity and mortality rates. Hence, the current investigation focusses to assess the antidiabetic potential of Sinigrin on diabetic animal model through the suppression of inflammation. Diabetes was initiated to the animals via administering streptozotocin (STZ) and supplemented with the Sinigrin at 25- and 50-mg/kg dose via oral route. The diabetic rats demonstrated the elevated glucose, food and water intake, kidney and liver weights, and reduced bodyweight and depleted insulin status. The Sinigrin treatment remarkably improved and modulated these changes in diabetic animals. Additionally, the Sinigrin supplementation also modulated the changes in glucose-6-phosphatase; fructose 1,6-bisphosphatase; AST; ALT; creatinine; and inflammatory mediators in the STZ-provoked diabetic animals. The levels of hexokinase, protein, and antioxidants also improved by the Sinigrin treatment. The histological investigations of pancreas also witnessed the therapeutic actions of Sinigrin, which is supported by the findings of biochemical examinations. Therefore, it was clear that the Sinigrin supplementation displayed remarkable antidiabetic effect on STZ-initiated diabetic animals via modulating inflammation and other biochemical changes, which recommends that Sinigrin could be a talented candidate for diabetes management in the future.
In vitro skin permeation of Sinigrin from its phytosome complex
J Pharm Pharmacol 2016 Dec;68(12):1577-1583.PMID:27696397DOI:10.1111/jphp.12594.
Objectives: Sinigrin is a major glucosinolate present in plants of the Brassicaceae family. Recently, Sinigrin and its phytosome formulations have been investigated for its wound-healing actions, by our research group. The aim of this study was to demonstrate Sinigrin drug release from its phytosome complex and also to determine whether the phytosome complex enhances the delivery of Sinigrin into the skin when compared to free Sinigrin. Methods: In vitro Franz cell diffusion studies were performed on human abdominal skin. The morphology of the phytosome complex was examined by transmission electron microscopy. The in vitro drug release was determined using dialysis sacks. Key findings: The in vitro drug release indicated a controlled and sustained release of Sinigrin from the phytosome complex. Tape stripping results showed that the sinigrin-phytosome complex (0.5155 μg/ml) statistically significantly enhanced the delivery of Sinigrin into the stratum corneum-epidermis when compared to the free Sinigrin (0.0730 μg/ml). Conclusions: These results suggested the possibility of utilizing sinigrin-phytosome complex, to optimally deliver Sinigrin to the skin which can be further used for various skin-related diseases including wound healing.
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.PMID:35993954DOI:10.1615/JEnvironPatholToxicolOncol.2022041136.
Breast carcinoma, one of the most lethal variants of carcinogenesis, significantly diagnosed type of cancer amongst the female population. Sinigrin, also known as glucosinolate, is found in the seeds of Brassica nigra and shown to enhance various cancer cells potentially. Nevertheless, the mechanistic explanation of Sinigrin (SGN)-mediated breast cancer growth and augmentation is still to be investigated. Therefore, we contended in this study that SGN impedes PI3K/AKT/mTOR phosphorylation-mediated cell cycle arrest in MCF-7 cells. SGN (20 M) was implemented to treat MCF-7 cells for 24 and 48 hours of incubation. A significant increase in cytotoxicity, reactive oxygen species (ROS) generation, cell cycle arrest, mitochondrion membrane alteration, lipid peroxidation, and antioxidant depletion was found in MCF-7 cells. The PI3K/AKT/mTOR events are crucial pathways that participate in survival, proliferation, and cell cycle regulation. Inhibition of PI3K/AKT/mTOR expression thought to be novel approach for alleviating breast cancer growth. We noticed that SGN inhibits PI3K, AKT, and mTOR phosphorylation, resulting in the downregulation of proliferative and cell cycle regulatory proteins, such as cyclin-Dl, PCNA, CDK4, and CDK6. SGN also causes apoptosis in MCF-7 cells by increasing nuclear fragmentation and by inducing pro-apoptotic gene expression. As a result, SGN inhibits breast cancer growth by impeding PI3K/AKT/mTOR phosphorylation-mediated cell cycle arrest in MCF-7 cells.