Sinigrin is an orally active thioglucoside found in cruciferous plants[1]. Sinigrin exhibits diverse activities, including anticancer, antibacterial, antifungal, anti-inflammatory, antioxidant, and lipogenesis-inhibitory effects[2]. Sinigrin is commonly used in research on tumors, inflammatory, and metabolic diseases[3].
In vitro, Sinigrin (1-100μg/mL; 8 days) dose-dependently inhibits 3T3-L1 adipogenesis, activated AMPK/ACC and suppressing MAPK phosphorylation, and blocked lipid accumulation, PPARγ/C/EBPα expression, and pro-inflammatory cytokine release without cytotoxicity[4]. Sinigrin (20μM; 24-48h) exerts potent cytotoxicity against MCF-7 breast cancer cells, blocked PI3K/AKT/mTOR phosphorylation, triggered S-phase arrest, ROS overload, mitochondrial depolarization, and caspase-9-mediated apoptosis while suppressing cyclin D1, CDK4/6, PCNA and Bcl-2[5].
In vitro, Sinigrin (20mg/kg/d; 28 days; oral gavage) reversed MCAO-induced neuronal apoptosis, oxidative stress and neurological deficits while suppressing TLR4/MyD88 signaling in Sprague–Dawley rats[6]. Sinigrin (30mg/kg; 12 days; oral gavage) reversed DSS-induced colitis in BALB/c mice, suppressed IL-6, IL-1β, TNF-α and IL-17, restored antioxidant enzymes, and inhibited MAPK phosphorylation[7].
References:
[1] Awasthi S, Saraswathi NT. Sinigrin, a major glucosinolate from cruciferous vegetables restrains non-enzymatic glycation of albumin. Int J Biol Macromol. 2016;83:410-415.
[2] Melrose J. The Glucosinolates: A Sulphur Glucoside Family of Mustard Anti-Tumour and Antimicrobial Phytochemicals of Potential Therapeutic Application. Biomedicines. 2019;7(3):62.
[3] Mazumder A, Dwivedi A, du Plessis J. Sinigrin and Its Therapeutic Benefits. Molecules. 2016;21(4):416.
[4] Lee HW, Rhee DK, Kim BO, Pyo S. Inhibitory effect of sinigrin on adipocyte differentiation in 3T3-L1 cells: Involvement of AMPK and MAPK pathways. Biomed Pharmacother. 2018;102:670-680.
[5] Li S, Lin J, Wei J, Zhou L, Wang P. 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.
[6] Guo S, Lei Q, Yang Q, Chen R. Sinigrin improves cerebral ischaemia-reperfusion injury by inhibiting the TLR4 pathway-mediated oxidative stress. Chem Biol Drug Des. 2024;103(2):e14480.
[7] Kotipalli RSS, Tirunavalli SK, Pote AB, et al. Sinigrin Attenuates the Dextran Sulfate Sodium-induced Colitis in Mice by Modulating the MAPK Pathway. Inflammation. 2023;46(3):787-807.
Sinigrin是一种存在于十字花科植物中的具有口服活性的硫代葡萄糖苷[1]。Sinigrin具有抗癌、抗菌、抗真菌、抗炎、抗氧化及抑制脂肪生成等多种活性[2]。Sinigrin常用于肿瘤、炎症性及代谢性疾病的研究[3]。
体外实验中，Sinigrin（1-100μg/mL；作用8天）可剂量依赖性地抑制3T3-L1前脂肪细胞分化，激活AMPK/ACC通路并抑制MAPK磷酸化，阻断脂质积累及PPARγ/C/EBPα表达，减少促炎细胞因子释放，且无细胞毒性[4]。Sinigrin（20μM；24-48小时）对MCF-7乳腺癌细胞具有显著细胞毒性，可阻断PI3K/AKT/mTOR磷酸化，诱导S期阻滞、ROS过载、线粒体去极化及caspase-9介导的凋亡，并下调cyclin D1、CDK4/6、PCNA和Bcl-2[5]。
体内实验中，Sinigrin（20mg/kg/d；28天；灌胃）可逆转Sprague–Dawley大鼠MCAO模型中的神经元凋亡、氧化应激及神经功能缺损，并抑制TLR4/MyD88信号通路[6]。Sinigrin（30mg/kg；12天；灌胃）可逆转BALB/c小鼠DSS诱导的结肠炎，抑制IL-6、IL-1β、TNF-α和IL-17，恢复抗氧化酶水平，并抑制MAPK磷酸化[7]。