Stachyose is an oligosaccharide and prebiotic[1]. Stachyose also serves as a specific inhibitor of PRDX5 (peroxiredoxin 5), acts directly on the PRDX5 protein, and inhibits its enzymatic activity[2]. Stachyose is commonly used in research on castration-resistant prostate cancer and metabolic diseases such as type 2 diabetes[3][4].
In vitro, Stachyose (0.4-3.2mg/mL in medium; 24h) dose-dependently inhibited Caco-2 colon cancer cells proliferation, induced cells apoptosis, decreased mitochondrial membrane potential, upregulated Bax, downregulated Bcl-2, promoted cytochrome C release, and activated caspases 3/9[5].
In vivo, Stachyose (200-600mg/kg/day; oral gavage for 3 weeks) dose-dependently alleviated DSS-induced colitis symptoms, increased tight junction protein expression (Occludin, Claudin-1, ZO-1), decreased pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), increased anti-inflammatory cytokine IL-10, and restored Treg/Th17 cell balance in a DSS-induced colitis mouse model[6]. Stachyose (1 or 5g/kg/day; oral gavage for 3 days) reduced myocardial infarction area and improved cardiac function in a mouse model of myocardial ischemia-reperfusion injury[7].
References:
[1] Li CN, Wang X, Lei L, et al. Berberine combined with stachyose induces better glycometabolism than berberine alone through modulating gut microbiota and fecal metabolomics in diabetic mice. Phytother Res. 2020;34(5):1166-1174.
[2] Wang R, Pan Y, Zhang L, et al. Prebiotic stachyose inhibits PRDX5 activity and castration-resistant prostate cancer development. Int J Biol Macromol. 2024;278(Pt 3):134844.
[3] Wang R, Mi Y, Ni J, et al. Identification of PRDX5 as A Target for The Treatment of Castration-Resistant Prostate Cancer. Adv Sci (Weinh). 2024;11(9):e2304939.
[4] Wu Y, Cao Y, Feng L, et al. The natural compound stachyose targets SGLT2-mediated metabolic reprogramming to ameliorate diabetic kidney disease. Phytomedicine. 2025;147:157182.
[5] Huang G, Mao J, Ji Z, Ailati A. Stachyose-induced apoptosis of Caco-2 cells via the caspase-dependent mitochondrial pathway. Food Funct. 2015;6(3):765-771.
[6] He N, Chen K, Yu S, et al. Stachyose Exerts Anticolitis Efficacy by Re-balancing Treg/Th17 and Activating the Butyrate-Derived PPARγ Signaling Pathway. J Agric Food Chem. 2024;72(21):12171-12183.
[7] Zhang AY, Su JB, Sun HT, et al. Stachyose ameliorates myocardial ischemia-reperfusion injury by inhibiting cardiomyocyte ferroptosis and macrophage pyroptosis. Int Immunopharmacol. 2024;143(Pt 1):113334.
Stachyose是一种寡糖，也是一种益生元[1]。Stachyose还作为PRDX5（过氧化物还原酶5）的特异性抑制剂，直接作用于PRDX5蛋白并抑制其酶活性[2]。Stachyose常用于去势抵抗性前列腺癌和2型糖尿病等代谢性疾病的研究[3][4]。
体外实验中，Stachyose（0.4-3.2mg/mL in medium；24小时）剂量依赖性地抑制了Caco-2结肠癌细胞的增殖，诱导细胞凋亡，降低了线粒体膜电位，上调了Bax蛋白，下调了Bcl-2蛋白，促进了细胞色素C的释放，并激活了caspase 3/9[5]。
体内实验中，在DSS诱导的结肠炎小鼠模型中，Stachyose（200-600 mg/kg/天；口服给药3周）剂量依赖性地减轻了DSS诱导的结肠炎症状，增加了紧密连接蛋白（Occludin、Claudin-1、ZO-1）的表达，降低了促炎细胞因子（TNF-α、IL-1β、IL-6）的水平，增加了抗炎细胞因子IL-10的水平，并恢复了Treg/Th17细胞的平衡[6]。Stachyose（1或5g/kg/天；口服给药3天）减少了心肌缺血再灌注损伤小鼠的心肌梗死面积，改善了小鼠的心脏功能[7]。