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]。