Sinapine
(Synonyms: 芥子碱) 目录号 : GC32906
Sinapine is an alkaloid isolated from seeds of the cruciferous species with antioxidant, antitumor and radio-protective activities. Sinapine inhibits the proliferation of Caco-2 cells via downregulation of P-glycoprotein.
Cas No.:18696-26-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | The Caco-2 cells are seeded into a 96-well plate with 8000 cells/well for 24 h. After incubation with different doses of Sinapine (0-200 μM), doxorubicin, or both for 24 h, the medium is discarded. Cell survival after exposure to Sinapine alone or a combination of Sinapine and the anti-tumor agent doxorubicin is examined by MTT colorimetric assay[1]. |
Animal experiment: | Rats[3]Sixty male Sprague-Dawley rats (95 g) are randomly allotted to 6 groups of 10 rats each and reared in individual cages. Six groups of 10 growing rats each are fed ad libitum for 15 days one of six diets: diet A, rapeseed (3.80 g of sinapine/kg DM); diet B, ethanol/water-extracted rapeseed (0.48 g of sinapine); diet C, control diet; diet G, control diet+3.74 g of extracted sinapine; diet H, control diet + 3.72 g of sinapine+other phenolic compounds; or diet I, control diet+the hydrolysis products of sinapine and other phenolic compounds. The rats are weighed at 8 a.m. on days 1, 4, 8, 11 and 15 of the trial. After sacrifice the gut contents are eliminated to permit determination of empty body weight gain (EBWG). The distribution, refusal and intake of each rat are recorded every day[3]. |
References: [1]. Guo Y, et al. Sinapine as an active compound for inhibiting the proliferation of Caco-2 cells via downregulation of P-glycoprotein. Food Chem Toxicol. 2014 May;67:187-92. | |
Sinapine is an alkaloid isolated from seeds of the cruciferous species with antioxidant, antitumor and radio-protective activities. Sinapine inhibits the proliferation of Caco-2 cells via downregulation of P-glycoprotein.
[1] Ying Guo, et al. Food Chem Toxicol. 2014 May;67:187-92.
| Cas No. | 18696-26-9 | SDF | |
| 别名 | 芥子碱 | ||
| Canonical SMILES | O=C(OCC[N+](C)(C)C)/C=C/C1=CC(OC)=C(O)C(OC)=C1 | ||
| 分子式 | C16H24NO5 | 分子量 | 310.36 |
| 溶解度 | DMSO: 250 mg/mL (805.52 mM) | 储存条件 | 4°C, away from moisture and 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 | 3.2221 mL | 16.1103 mL | 32.2206 mL |
| 5 mM | 0.6444 mL | 3.2221 mL | 6.4441 mL |
| 10 mM | 0.3222 mL | 1.611 mL | 3.2221 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。
Sinapine improves LPS-induced oxidative stress in hepatocytes by down-regulating MCJ protein expression
Life Sci 2022 Oct 1;306:120828.PMID:35872005DOI:10.1016/j.lfs.2022.120828.
Oxidative stress is an important part of the development of NAFLD, and hepatic injury can be prevented by inhibiting oxidative stress. In this study, we investigated the potential role of Sinapine in protecting the liver. LPS was selected to establish the oxidative stress model of THLE-2 cells, and the treatment concentrations of LPS (5 μg/mL) and Sinapine (5 μM, 20 μM, and 80 μM) were determined by toxicity experiments. The MDA of the Sinapine (80 μM) pretreatment group was 1.09 ± 0.13 nmol/mg prot which was reduced by 27.67 % compared with the LPS group. Furthermore, SOD and GSH-Px levels were significantly increased by 40.61 % and 49.60 %, respectively. And the ROS levels of 20 and 80 μM Sinapine were reduced by 31.47 % and 40.31 %, respectively (p < 0.01) compared with the model group. The mitochondrial membrane potential had similar results. It was also found that Sinapine can significantly down-regulate the level of MCJ protein (p < 0.01), which is related to oxidative stress. Our results indicate that Sinapine can maintain liver health by down-regulating the expression of MCJ protein to inhibit oxidative stress, which provides a theoretical basis for the use of Sinapine as an inhibitor of MCJ.
Sinapine, but not sinapic acid, counteracts mitochondrial oxidative stress in cardiomyocytes
Redox Biol 2020 Jul;34:101554.PMID:32464499DOI:10.1016/j.redox.2020.101554.
Introduction: When confronted to stress or pathological conditions, the mitochondria overproduce reactive species that participate in the cellular dysfunction. These organelles are however difficult to target with antioxidants. A feature of mitochondria that can be used for this is the negatively charged compartments they form. Most of mitochondrion-targeting antioxidants are therefore cationic synthetic molecules. Our hypothesis is that such mitochondriotropic traits might also exists in natural molecules. Aim: We tested here whether Sinapine, a natural phenolic antioxidant-bearing a permanent positive charge, can target mitochondria to modulate mitochondrial oxidative stress. Methods: Experiments were performed in-vitro, in-cellulo, ex-vivo, and in-vivo, using cardiac tissue. The sinapic acid -lacking the positively-charged-choline-moiety present in sinapine-was used as a control. Sinapine entry into mitochondria was investigated in-vivo and in cardiomyocytes. We used fluorescent probes to detect cytosolic (H2DCFDA) and mitochondrial (DHR123) oxidative stress on cardiomyocytes induced with either hydrogen peroxide (H2O2) or antimycin A, respectively. Finally, ROS production was measured with DHE 10 min after ischemia-reperfusion (IR) on isolated heart, treated or not with Sinapine, sinapic acid or with a known synthetic mitochondrion-targeted antioxidant (mitoTempo). Results: We detected the presence of Sinapine within mitochondria in-vitro, after incubation of isolated cardiomyocytes, and in-vivo, after oral treatment. The presence of sinapic acid was not detected in the mitochondria. Both the Sinapine and the sinapic acid limited cytosolic oxidative stress in response to H2O2. Only Sinapine was able to blunt oxidative stress resulting from antimycin A-induced mtROS. Both mitoTempo and Sinapine improved cardiac functional recovery following IR. This was associated with lower ROS production within the cardiac tissue. Conclusion: Sinapine, a natural cationic hydrophilic phenol, commonly and substantially found in rapeseed species, effectively (i) enters within the mitochondria, (ii) selectively decreases the level of mitochondrial oxidative stress and, (iii) efficiently limits ROS production during cardiac ischemia-reperfusion.
Sinapine-enriched rapeseed oils reduced fatty liver formation in high-fat diet-fed C57BL/6J mice
RSC Adv 2020 Jun 3;10(36):21248-21258.PMID:35518778DOI:10.1039/d0ra00215a.
Oil enrichment with trace amounts of components has significant effects on animal nutrition and health. In this work, the potential impact of Sinapine, a trace amount of polyphenol naturally present in rapeseeds, was investigated in high-fat diet (HF)-fed C57BL/6J mice. The mice were fed with different diets including chow diet (LF), HF diet, rapeseed oil-containing HF diet (RO), and rapeseed oils enriched with Sinapine (500 mg kg-1 oil, high-fat diet, RP) for 12 weeks. Here, it was demonstrated that Sinapine supplementation significantly reduced (P < 0.05) body weight increase, fat accumulation, and fatty liver formation in mice when compared with those fed with a high-fat diet. The TG, LDL-C, ALT and AST levels in the RP group were significantly reduced (P < 0.05) by 15.67%, 73.62%, 20.67%, and 31.58%, respectively, compared with that in the HF group. Besides, the addition of Sinapine prevented the degeneration of mouse adipocytes and lipid accumulation in the liver. Moreover, this change was achieved by downregulating SREBP-1c and FAS and upregulating PPAR-α and ACOX1 gene expression levels. Our results indicate that Sinapine can be used as a prebiotic to enhance the nutritional function of vegetable oils to prevent obesity-related chronic diseases such as NAFLD.
Sinapine as an active compound for inhibiting the proliferation of Caco-2 cells via downregulation of P-glycoprotein
Food Chem Toxicol 2014 May;67:187-92.PMID:24607798DOI:10.1016/j.fct.2014.02.035.
Sinapine, an alkaloid from seeds of the cruciferous species, shows favorable biological activities such as antioxidant and radio-protective activities. However, the inhibitory effect of Sinapine on tumors, and the molecular mechanisms have not been completely understood thus far. In this study, we determined anti-proliferative effects of Sinapine. We examined the anti-tumor effects of the combination of Sinapine and doxorubicin. The results of the MTT assay and apoptosis showed that Sinapine increased the sensitivity of Caco-2 cells to doxorubicin in a dose-dependent manner, whereas no or less effect was observed in the cells treated with doxorubicin alone. The combination of Sinapine and doxorubicin had a synergistic effect and increased the cytotoxicity of doxorubicin against Caco-2 cells. Doxorubicin accumulation assay showed that Sinapine increased the intracellular accumulation of doxorubicin in dose-dependent manner. Immunoblotting and QT-PCR analysis showed that Sinapine suppressed P-glycoprotein (P-gp) expression via ubiquitination. A significant correlation was observed between the expression of p-ERK1/2 and P-gp. These results indicated that Sinapine played an important role in the down-regulation of P-gp expression through suppression of FGFR4-FRS2α-ERK1/2 signaling pathway. To our knowledge, this is the first study to show that Sinapine can be used as an effective natural compound for chemo-resistance.
Sinapine Thiocyanate Inhibits the Proliferation and Mobility of Pancreatic Cancer Cells by Up-Regulating GADD45A
J Cancer 2022 Jan 24;13(4):1229-1240.PMID:35281859DOI:10.7150/jca.65212.
Background: Sinapine thiocyanate (ST), an alkaloid isolated from the seeds of cruciferous species, has exhibited anti-inflammatory, anti-malignancy, and anti-angiogenic effects in previous studies. However, the effects and molecular mechanisms of action of ST in pancreatic cancer (PC) are still limited. Materials and methods: PC cells were treated with different concentrations (0, 20, 40, and 80 μM) of ST. The proliferative ability of PC cells in vitro was determined using cell count kit-8 (CCK-8), 5-ethynyl-2' deoxyuridine, colony formation, and flow cytometry assays. The mobility of PC cells in vitro was analyzed using wound healing assay, transwell assay, Western blotting, and immunofluorescence. High-throughput sequencing followed by bioinformatics analysis, reverse-transcriptase quantitative polymerase chain reaction (RT-qPCR), and Western blotting were performed to identify the key targets of ST. Finally, CCK-8 assay, wound healing assay, and xenograft tumor model were used to determine the relationship between ST and growth arrest and DNA damage-inducible alpha (GADD45A; the key target of ST) and malignant biological properties of PC in vitro and in vivo. Results: ST significantly repressed the PC cell proliferation rate and colony formation in vitro and arrested cells in the G2/M phase. ST inhibited PC cell mobility in vitro and increased E-cadherin expression (an epithelial biomarker). GADD45A was considered the key target of ST in PC and was elevated in PC cells treated with ST. The inhibition of GADD45A significantly alleviated the suppressive effects of ST on PC cell proliferation and mobility in vitro. ST suppressed PC cell proliferation in vivo and increased GADD45A expression in tumor tissues. Conclusion: ST exhibited significant anti-tumor effects on PC cells by upregulating GADD45A. ST may be a potential drug for PC treatment.