L-Sulforaphane
(Synonyms: L-萝卜硫素,L-Sulforaphane) 目录号 : GC41554
L-Sulforaphane是一种具有口服活性的非特异性核因子E2相关因子2(Nrf2)激活剂,其通过抑制Keap1蛋白与Nrf2的相互作用发挥功能。
Cas No.:142825-10-3
Sample solution is provided at 25 µL, 10mM.
L-Sulforaphane is an orally active, non-specific activator of nuclear factor erythroid 2-related factor 2 (Nrf2), which functions by inhibiting the interaction between Keap1 protein and Nrf2[1]. L-Sulforaphane is widely used in research on oxidative stress, inflammation, and related signaling pathways, with extensive applications in areas such as cancer chemoprevention and neuroprotection [2]. Additionally, L-Sulforaphane demonstrates inhibitory activity against histone deacetylase (HDAC) with an IC₅₀ value of 8.7μM[3].
In macrophages, L-Sulforaphane (10μM; 24h) can induce human monocyte-derived macrophages to differentiate from a pro-inflammatory M1 phenotype to an anti-inflammatory M2 phenotype [4]. L-Sulforaphane (5-50μM; 24h) treatment of porcine monocyte-derived dendritic cells (moDCs), under lipopolysaccharide (LPS) stimulation, inhibits their differentiation into mature moDCs and increases their phagocytic capacity [5].
In the TRAMP model, L-Sulforaphane (10mg/mL; po; 17-19 week) protects mice from prostate cancer by increasing the secretion of interleukin (IL)-12 by dendritic cells, thereby promoting the infiltration of CD57+ cytotoxic natural killer (NK) cells and CD3+ T cells[6]. In a mouse model of chronic allergic airway disease induced by ovalbumin (OVA), L-Sulforaphane (25mg/mL; po; 9 week) reversed OVA-induced epithelial thickening, collagen deposition, goblet cell metaplasia, and inflammation [7].
References:
[1]. Ruhee R T, Suzuki K. The immunomodulatory effects of Sulforaphane in exercise-induced inflammation and oxidative stress: A prospective nutraceutical[J]. International journal of molecular sciences, 2024, 25(3): 1790.
[2]. Alves I, Araújo E M Q, Dalgaard L T, et al. Protective effects of sulforaphane preventing inflammation and oxidative stress to enhance metabolic health: a narrative review[J]. Nutrients, 2025, 17(3): 428.
[3]. Tortorella S M, Royce S G, Licciardi P V, et al. Dietary sulforaphane in cancer chemoprevention: the role of epigenetic regulation and HDAC inhibition[J]. Antioxidants & redox signaling, 2015, 22(16): 1382-1424.
[4]. Pal S, Konkimalla V B. Sulforaphane regulates phenotypic and functional switching of both induced and spontaneously differentiating human monocytes[J]. International immunopharmacology, 2016, 35: 85-98.
[5]. Qu X, Pröll M, Neuhoff C, et al. Sulforaphane epigenetically regulates innate immune responses of porcine monocyte-derived dendritic cells induced with lipopolysaccharide[J]. PLoS one, 2015, 10(3): e0121574.
[6]. Singh S V, Warin R, Xiao D, et al. Sulforaphane inhibits prostate carcinogenesis and pulmonary metastasis in TRAMP mice in association with increased cytotoxicity of natural killer cells[J]. Cancer research, 2009, 69(5): 2117-2125
[7]. Royce S G, Licciardi P V, Beh R C, et al. Sulforaphane prevents and reverses allergic airways disease in mice via anti-inflammatory, antioxidant, and epigenetic mechanisms[J]. Cellular and Molecular Life Sciences, 2022, 79(11): 579.
L-Sulforaphane是一种具有口服活性的非特异性核因子E2相关因子2(Nrf2)激活剂,其通过抑制Keap1蛋白与Nrf2的相互作用发挥功能[1]。L-Sulforaphane广泛应用于氧化应激、炎症及相关信号通路研究,在癌症化学预防和神经保护等领域具有重要应用价值[2]。此外,L-Sulforaphane对组蛋白去乙酰化酶(HDAC)具有抑制活性,其IC₅₀值为8.7μM[3]。
在巨噬细胞中,L-Sulforaphane(10μM;24h)能够诱导人单核细胞来源的巨噬细胞从促炎性M1表型向抗炎性M2表型分化[4]。在脂多糖(LPS)刺激条件下,L-Sulforaphane(5-50μM;24h)处理猪单核细胞来源的树突状细胞(moDCs)可抑制其向成熟moDCs的分化,并增强其吞噬能力[5]。
在TRAMP前列腺癌模型中,L-Sulforaphane(10mg/mL;po;17-19周)通过增强树突状细胞分泌白细胞介素(IL)-12,从而促进CD57+细胞毒性自然杀伤(NK)细胞和CD3+ T细胞的浸润,可有效预防前列腺癌发生[6]。在卵清蛋白(OVA)诱导的慢性过敏性气道疾病小鼠模型中,L-Sulforaphane(25mg/mL;po;9周)能够逆转OVA诱导的上皮增厚、胶原沉积、杯状细胞化生及炎症反应[7]。
| Cell experiment [1]: | |
Cell lines | THP-1 cells |
Preparation Method | THP-1 cells were maintained with RPMI-1640 media supplemented with 10% Fetal Bovine Serum, 10mM HEPEs, 1% Penicillin-streptomycin, at 37 °C, 5% CO2. THP-1 cells (1×105cells/mL) were treated with 10µM and 50µM L-Sulforaphane for 6h, 24h and 48h. A control group with R10 media only and a DMSO-only group was used as the vehicle control group for each experiment. Viability of THP-1 monocytes was measured using trypan blue exclusion dye at each timepoint. |
Reaction Conditions | 10-50μM; 24-48h |
Applications | L-Sulforaphane (10-50μM; 24-48h) Increases Nrf2-ARE Activity in THP-1 Monocytes |
| Animal experiment [2]: | |
Animal models | TRAMP (Transgenic Adenocarcinoma of the Mouse Prostate) model |
Preparation Method | TRAMP mice were maintained in a climate-controlled environment with a 12h light/12h dark cycle and fed food and water. At 6 to 7 wk of age, mice were randomized into two groups. Mice in the control group received 0.1mL PBS by oral gavage thrice per week, whereas the experimental mice received 10mg/mL L-Sulforaphane by oral gavage thrice per week for 17 to 19 wk. Body weights of the control and L-Sulforaphane -treated mice were recorded once each week beginning at the onset of the study. |
Dosage form | 10mg/mL; po; 17-19 week |
Applications | L-Sulforaphane protects mice from prostate cancer by increasing the secretion of interleukin (IL)-12 from dendritic cells, thereby promoting the infiltration of CD57+ cytotoxic natural killer (NK) cells and CD3+ T cells. |
References: | |
| Cas No. | 142825-10-3 | SDF | |
| 别名 | L-萝卜硫素,L-Sulforaphane | ||
| Canonical SMILES | C[S@](CCCCN=C=S)=O | ||
| 分子式 | C6H11NOS2 | 分子量 | 177.3 |
| 溶解度 | DMF: 3 mg/ml,DMSO: 16 mg/ml,Ethanol: 20 mg/ml,PBS (pH 7.2): 10 mg/ml | 储存条件 | -20°C, protect from light |
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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 | 564 μL | 2.8201 mL | 5.6402 mL |
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