Sulforaphane
(Synonyms: 萝卜硫素) 目录号 : GC14016
萝卜硫素 (SFN) 称为 [1-isothiocyanato-4-(methylsulfinyl)butane]。
Cas No.:4478-93-7
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >97.00%
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- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
HepaRG cells |
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Preparation Method |
HepaRG cells at a concentration of 1.5 104 cells/mL were seeded on uncoated plastic tissue culture dishes and treated with sulforaphane at different concentrations (0 -40 uM) over a time course (12-48 h). The cells as well as the homogenates from liver tissues were solubilized, and the activity solution including a reporter dye were added to the supernatants. |
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Reaction Conditions |
0 -40 uM sulforaphane for 12-48 h |
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Applications |
Sulforaphane amplifies ALDH2 activity in HepaRG cells and suppresses acetaldehyde-induced proliferation and activation in LX-2 cells. |
| Animal experiment [2]: | |
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Animal models |
Ten-week-old female C57BL/6J mice |
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Preparation Method |
Mice in the CD/ CCl4 group were fed the normal liquid diet and received 1 mL/kg body weight CCl4 dissolved in corn oil by intraperitoneal injection twice weekly. Mice in the ED/ CCl4 group were fed a 2.5% (v/v) ethanol-containing Lieber-DeCarli liquid diet (Research Diets) (ED) and received intraperitoneal CCl4 injection twice weekly (1 mL/kg body weight). Mice in the ED/ CCl4/SFN group were fed the ED with sulforaphane and received intraperitoneal CCl4 injection (1 mL/kg body weight) twice weekly; in this group, sulforaphane was administered peroral as a mixture of ED (5 µmoL/d/body weight). |
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Dosage form |
Sulforaphane was administered peroral as a mixture of ED (5 µmoL/d/body weight) twice weekly |
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Applications |
Sulforaphane exerts antioxidative effects with ALDH2 induction in liver fibrosis induced by ethanol exposure in CCl4-treated mice. |
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References: [1]. Ishida K, Kaji K, et,al. Sulforaphane ameliorates ethanol plus carbon tetrachloride-induced liver fibrosis in mice through the Nrf2-mediated antioxidant response and acetaldehyde metabolization with inhibition of the LPS/TLR4 signaling pathway. J Nutr Biochem. 2021 Mar;89:108573. doi: 10.1016/j.jnutbio.2020.108573. Epub 2020 Dec 31. PMID: 33388347. |
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Sulforaphane (SFN) known as [1-isothiocyanato-4-(methylsulfinyl)butane]. It is an isothiocyanate that is present naturally in widely consumed vegetables and has a particularly high concentration in broccoli[1,10]. Sulforaphane is a phytocompound with antioxidant, anti-inflammatory, and antiapoptotic effects[2].
Sulforaphane amplifies ALDH2 activity in HepaRG cells and suppresses acetaldehyde-induced proliferation and activation in LX-2 cells[3]. Sulforaphane reversed mesenchymal-like changes induced by TGF-β1 and restored cells to their epithelial-like morphology. The expression of the epithelial marker, E-cadherin, increased after Sulforaphane treatment, while expression of the mesenchymal markers, N-cadherin, vimentin, and α-SMA decreased in A549 cells after SFN treatment[4]. Sulforaphane inhibited cell growth and reduced collagen at the mRNA and protein levels in keloid fibroblasts. Moreover, sulforaphane markedly suppressed the expression of IL-6 and α-SMA and inhibited Stat3 and Smad3 signaling pathways in keloid fibroblast KF112 cells[8]. Sulforaphane inhibited XWLC-05 cell growth with inhibitory concentration (IC)50 of 4.04, 3.38, and 3.02 μg/mL at 24, 48, and 72 hours, respectively. Sulforaphane affected the XWLC-05 cell cycle as cells accumulated in the G2/M phase[9].
Sulforaphane exerts antioxidative effects with ALDH2 induction in liver fibrosis induced by ethanol exposure in CCl4-treated mice[3]. Nrf2 plays the indispensable role for Sulforaphane cardiac protection from T2DM with significant induction of MT and other antioxidants. MT expression induced by Sulforaphane is Nrf2 dependent, but is not indispensable for SFN-induced cardiac protection from T2DM[5]. Sulforaphane significantly reduced the incidence and size of 4NQO-induced tongue tumors in mice[6]. Sulforaphane suppresses skin cancer via blocking sulfatase-2 with subsequent elevation in HSPGs and reduction in glypican-3. Moreover, sulforaphane attenuated skin cancer-induced activation of inflammatory and apoptotic pathways[7].
References:
[1]. Panjwani AA, Liu H, et,al. Crucifers and related vegetables and supplements for neurologic disorders: what is the evidence? Curr Opin Clin Nutr Metab Care. 2018 Nov;21(6):451-457. doi: 10.1097/MCO.0000000000000511. PMID: 30199394.
[2]. Schepici G, Bramanti P, et,al. Efficacy of Sulforaphane in Neurodegenerative Diseases. Int J Mol Sci. 2020 Nov 16;21(22):8637. doi: 10.3390/ijms21228637. PMID: 33207780; PMCID: PMC7698208.
[3]. Ishida K, Kaji K, et,al. Sulforaphane ameliorates ethanol plus carbon tetrachloride-induced liver fibrosis in mice through the Nrf2-mediated antioxidant response and acetaldehyde metabolization with inhibition of the LPS/TLR4 signaling pathway. J Nutr Biochem. 2021 Mar;89:108573. doi: 10.1016/j.jnutbio.2020.108573. Epub 2020 Dec 31. PMID: 33388347.
[4]. Kyung SY, Kim DY, et,al. Sulforaphane attenuates pulmonary fibrosis by inhibiting the epithelial-mesenchymal transition. BMC Pharmacol Toxicol. 2018 Apr 2;19(1):13. doi: 10.1186/s40360-018-0204-7. PMID: 29609658; PMCID: PMC5879815.
[5]. Gu J, Cheng Y, et,al. Metallothionein Is Downstream of Nrf2 and Partially Mediates Sulforaphane Prevention of Diabetic Cardiomyopathy. Diabetes. 2017 Feb;66(2):529-542. doi: 10.2337/db15-1274. Epub 2016 Nov 30. PMID: 27903744; PMCID: PMC5248986.
[6]. Bauman JE, Zang Y, et,al. Prevention of Carcinogen-Induced Oral Cancer by Sulforaphane. Cancer Prev Res (Phila). 2016 Jul;9(7):547-57. doi: 10.1158/1940-6207.CAPR-15-0290. Epub 2016 Jun 23. PMID: 27339168; PMCID: PMC4930727.
[7]. Alyoussef A, Taha M. Antitumor activity of sulforaphane in mice model of skin cancer via blocking sulfatase-2. Exp Dermatol. 2019 Jan;28(1):28-34. doi: 10.1111/exd.13802. Epub 2018 Dec 11. PMID: 30315662.
[8]. Kawarazaki A, Horinaka M, et,al. Sulforaphane suppresses cell growth and collagen expression of keloid fibroblasts. Wound Repair Regen. 2017 Apr;25(2):224-233. doi: 10.1111/wrr.12512. Epub 2017 Feb 20. PMID: 28120534.
[9]. Zhou L, Yao Q, et,al. Sulforaphane-induced apoptosis in Xuanwei lung adenocarcinoma cell line XWLC-05. Thorac Cancer. 2017 Jan;8(1):16-25. doi: 10.1111/1759-7714.12396. Epub 2016 Nov 23. PMID: 27878984; PMCID: PMC5217876.
[10].Gamet-Payrastre L, Li P, et,al. Sulforaphane, a naturally occurring isothiocyanate, induces cell cycle arrest and apoptosis in HT29 human colon cancer cells. Cancer Res. 2000 Mar 1;60(5):1426-33. PMID: 10728709.
萝卜硫素 (SFN) 称为 [1-isothiocyanato-4-(methylsulfinyl)butane]。它是一种异硫氰酸酯,天然存在于广泛食用的蔬菜中,在西兰花中含量特别高[1,10]。萝卜硫素是一种具有抗氧化、抗炎和抗细胞凋亡作用的植物化合物[2]。
萝卜硫素可增强 HepaRG 细胞中的 ALDH2 活性并抑制乙醛诱导的 LX-2 细胞增殖和活化[3]。萝卜硫素可逆转 TGF-β1 诱导的间充质样变化,并将细胞恢复到上皮样形态。 SFN 处理后 A549 细胞上皮标志物 E-cadherin 的表达增加,而间充质标志物 N-cadherin、vimentin 和 α-SMA 的表达减少[4] .萝卜硫素抑制细胞生长并减少瘢痕疙瘩成纤维细胞 mRNA 和蛋白质水平的胶原蛋白。此外,萝卜硫素显着抑制瘢痕疙瘩成纤维细胞KF112细胞IL-6和α-SMA的表达,抑制Stat3和Smad3信号通路[8]。萝卜硫素抑制 XWLC-05 细胞生长,抑制浓度 (IC)50 在 24、48 和 72 小时时分别为 4.04、3.38 和 3.02 μg/mL。萝卜硫素影响XWLC-05细胞周期,细胞在G2/M期聚集[9]。
在 CCl4 处理的小鼠中,萝卜硫素通过 ALDH2 诱导在乙醇暴露诱导的肝纤维化中发挥抗氧化作用[3]。 Nrf2 通过显着诱导 MT 和其他抗氧化剂,在萝卜硫素心脏保护免受 T2DM 方面发挥着不可或缺的作用。萝卜硫素诱导的 MT 表达依赖于 Nrf2,但对于 SFN 诱导的 T2DM 心脏保护作用并非必不可少[5]。萝卜硫素显着降低了 4NQO 诱导的小鼠舌肿瘤的发生率和大小[6]。萝卜硫素通过阻断 sulfatase-2 并随后升高 HSPG 和减少 glypican-3 来抑制皮肤癌。此外,萝卜硫素减弱了皮肤癌诱导的炎症和细胞凋亡通路的激活[7]。
| Cas No. | 4478-93-7 | SDF | |
| 别名 | 萝卜硫素 | ||
| 化学名 | 1-isothiocyanato-4-(methylsulfinyl)-butane | ||
| Canonical SMILES | CS(CCCCN=C=S)=O | ||
| 分子式 | C6H11NOS2 | 分子量 | 177.3 |
| 溶解度 | ≥ 67.6mg/mL in DMSO | 储存条件 | Store at -20°C, sealed storage, 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 | 5.6402 mL | 28.2008 mL | 56.4016 mL |
| 5 mM | 1.128 mL | 5.6402 mL | 11.2803 mL |
| 10 mM | 0.564 mL | 2.8201 mL | 5.6402 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。
Isothiocyanate from Broccoli, Sulforaphane, and Its Properties
J Med Food2019 Feb;22(2):121-126.PMID: 30372361DOI: 10.1089/jmf.2018.0024
Sulforaphane is an isothiocyanate occurring in stored form as glucoraphanin in cruciferous vegetables such as cabbage, cauliflower, and kale, and at high levels in broccoli especially in broccoli sprouts. Glucoraphanin requires the plant enzyme myrosinase for converting it into sulforaphane. Sulforaphane is metabolized through mercapturic acid pathway, being conjugated with glutathione and undergoes further biotransformation, yielding metabolites. Sulforaphane is extensively investigated and is in the interest in medicine for its health benefits. It has been shown that sulforaphane may protect against various types of cancer, may also decrease the risk of cardiovascular disease, and help in autism and osteoporosis. Our review offers a short summary of interesting properties of sulforaphane. Both the in vitro and in vivo methods/models and clinical studies are mentioned.
Efficacy of Sulforaphane in Neurodegenerative Diseases
Int J Mol Sci2020 Nov 16;21(22):8637.PMID: 33207780DOI: 10.3390/ijms21228637
Sulforaphane (SFN) is a phytocompound belonging to the isothiocyanate family. Although it was also found in seeds and mature plants, SFN is mainly present in sprouts of many cruciferous vegetables, including cabbage, broccoli, cauliflower, and Brussels sprouts. SFN is produced by the conversion of glucoraphanin through the enzyme myrosinase, which leads to the formation of this isothiocyanate. SFN is especially characterized by antioxidant, anti-inflammatory, and anti-apoptotic properties, and for this reason, it aroused the interest of researchers. The aim of this review is to summarize the experimental studies present on Pubmed that report the efficacy of SFN in the treatment of neurodegenerative disease, including Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Therefore, thanks to its beneficial effects, SFN could be useful as a supplement to counteracting neurodegenerative diseases.
Nrf2 targeting by sulforaphane: A potential therapy for cancer treatment
Crit Rev Food Sci Nutr2018 May 24;58(8):1391-1405.PMID: 28001083DOI: 10.1080/10408398.2016.1259983
In the past decades, extensive studies have reported the potential chemopreventive activity of sulforaphane, an isothiocyanate derived from glucoraphanin, occurring in large amounts in Brassica genus plants. Sulforaphane was found to be active against several forms of cancer. A growing body of data shows that sulforaphane acts against cancer at different levels, from development to progression, through pleiotropic effects. In this review, we discuss the available experimental and clinical data on the potential therapeutic role of sulforaphane against cancer. Its effects range from the protection of cells from DNA damage to the modulation of the cell cycle via pro-apoptotic, anti-angiogenesis and anti-metastasis activities. At molecular level, sulforaphane modulates cellular homeostasis via the activation of the transcription factor Nrf2. Although data from clinical studies are limited, sulforaphane remains a good candidate in the adjuvant therapy based on natural molecules against several types of cancer.
Sulforaphane treatment of autism spectrum disorder (ASD)
Proc Natl Acad Sci U S A2014 Oct 28;111(43):15550-5.PMID: 25313065DOI: 10.1073/pnas.1416940111
Autism spectrum disorder (ASD), characterized by both impaired communication and social interaction, and by stereotypic behavior, affects about 1 in 68, predominantly males. The medico-economic burdens of ASD are enormous, and no recognized treatment targets the core features of ASD. In a placebo-controlled, double-blind, randomized trial, young men (aged 13-27) with moderate to severe ASD received the phytochemical sulforaphane (n = 29)--derived from broccoli sprout extracts--or indistinguishable placebo (n = 15). The effects on behavior of daily oral doses of sulforaphane (50-150 ?mol) for 18 wk, followed by 4 wk without treatment, were quantified by three widely accepted behavioral measures completed by parents/caregivers and physicians: the Aberrant Behavior Checklist (ABC), Social Responsiveness Scale (SRS), and Clinical Global Impression Improvement Scale (CGI-I). Initial scores for ABC and SRS were closely matched for participants assigned to placebo and sulforaphane. After 18 wk, participants receiving placebo experienced minimal change (<3.3%), whereas those receiving sulforaphane showed substantial declines (improvement of behavior): 34% for ABC (P < 0.001, comparing treatments) and 17% for SRS scores (P = 0.017). On CGI-I, a significantly greater number of participants receiving sulforaphane had improvement in social interaction, abnormal behavior, and verbal communication (P = 0.015-0.007). Upon discontinuation of sulforaphane, total scores on all scales rose toward pretreatment levels. Dietary sulforaphane, of recognized low toxicity, was selected for its capacity to reverse abnormalities that have been associated with ASD, including oxidative stress and lower antioxidant capacity, depressed glutathione synthesis, reduced mitochondrial function and oxidative phosphorylation, increased lipid peroxidation, and neuroinflammmation.
Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma
Int J Mol Sci2021 May 31;22(11):5938.PMID: 34073079DOI: 10.3390/ijms22115938
Sulforaphane (SFN) is a natural glucosinolate found in cruciferous vegetables that acts as a chemopreventive agent, but its mechanism of action is not clear. Due to antioxidative mechanisms being thought central in preventing cancer progression, SFN could play a role in oxidative processes. Since redox imbalance with increased levels of reactive oxygen species (ROS) is involved in the initiation and progression of bladder cancer, this mechanism might be involved when chemoresistance occurs. This review summarizes current understanding regarding the influence of SFN on ROS and ROS-related pathways and appraises a possible role of SFN in bladder cancer treatment.