Stachyose (hydrate)
(Synonyms: 水苏糖) 目录号 : GC49227
An oligosaccharide and prebiotic
Cas No.:54261-98-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Stachyose is an oligosaccharide and prebiotic.1,2,3 In vivo, stachyose (1 g/kg per day) reduces the number of colonic lesions and serum TNF-α, IL-6, IL-10, and IL-17a levels, as well as increases gut levels of Akkermansia and the probiotic Lactobacillus, in a rat model of colitis induced by dextran sulfate .1 It decreases serum LPS, IL-6, and TNF-α levels and enriches Phascolarctobacterium, Bilophila, Oscillospira, and Turicibacter in the gut microbiota in a rat model of diabetes induced by high-fat diet and streptozotocin .2 Stachyose also enhances berberine-induced blood glucose control and improvements in insulin resistance, as well as decreases the fecal concentration of short-chain fatty acids, in the KKAγ mouse model of type 2 diabetes.3
1.He, L., Zhang, F., Jian, Z., et al.Stachyose modulates gut microbiota and alleviates dextran sulfate sodium-induced acute colitis in miceSaudi J. Gastroenterol.26(3)153-159(2020) 2.Liu, G., Bei, J., Liang, L., et al.Stachyose improves inflammation through modulating gut microbiota of high-fat diet/streptozotocin-induced type 2 diabetes in ratsMol. Nutr. Food Res.62(6)e1700954(2018) 3.Cao, H., Li, C., Lei, L., et al.Stachyose improves the effects of berberine on glucose metabolism by regulating intestinal microbiota and short-chain fatty acids in spontaneous type 2 diabetic KKAy miceFront. Pharmacol.11578943(2020)
| Cas No. | 54261-98-2 | SDF | |
| 别名 | 水苏糖 | ||
| Canonical SMILES | OC[C@]1(O[C@@H]([C@H]([C@@H]1O)O)CO)O[C@H]2O[C@@H]([C@H]([C@@H]([C@H]2O)O)O)CO[C@H]3O[C@@H]([C@@H]([C@@H]([C@H]3O)O)O)CO[C@H]4O[C@@H]([C@@H]([C@@H]([C@H]4O)O)O)CO.O | ||
| 分子式 | C24H42O21·XH2O | 分子量 | 666.6 |
| 溶解度 | DMSO: 1 mg/ml,PBS (pH 7.2): 10 mg/ml | 储存条件 | -20°C |
| 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 | 1.5002 mL | 7.5008 mL | 15.0015 mL |
| 5 mM | 0.3 mL | 1.5002 mL | 3.0003 mL |
| 10 mM | 0.15 mL | 0.7501 mL | 1.5002 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。
The role of functional oligosaccharides as prebiotics in ulcerative colitis
Food Funct 2022 Jul 4;13(13):6875-6893.PMID:35703137DOI:10.1039/d2fo00546h.
The incidence rate of ulcerative colitis (UC) has increased significantly over the past decades and it places an increasing burden on health and social systems. The current studies on UC implicate a strong correlation between host gut microbiota immunity and the pathogenesis of UC. Meanwhile, more and more functional oligosaccharides have been reported as prebiotics to alleviate UC, since many of them can be metabolized by gut microbiota to produce short-chain fatty acids (SCFAs). The present review is focused on the structure, sources and specific applications of various functional oligosaccharides related to the prevention and treatment of UC. The available evidence for the usage of functional oligosaccharides in UC treatment are summarized, including fructo-oligosaccharides (FOS), galacto-oligosaccharides (GOS), chito-oligosaccharides (COS), alginate-oligosaccharides (AOS), xylooligosaccharides (XOS), Stachyose and inulin.
Tempol ameliorates polycystic ovary syndrome through attenuating intestinal oxidative stress and modulating of gut microbiota composition-serum metabolites interaction
Redox Biol 2021 May;41:101886.PMID:33592539DOI:10.1016/j.redox.2021.101886.
Polycystic ovary syndrome (PCOS) is a complex endocrine and metabolic disorder, which is often accompanied by oxidative stress. Tempol, a superoxide dismutase mimetic, protects against several diseases caused by oxidative stress. However, the effect of tempol on PCOS has not been investigated. The present study demonstrated the alleviation of ovarian dysfunction and glucose tolerance in dehydroepiandrosterone (DHEA)-induced PCOS rats treated with tempol. Tempol significantly reduced the intestinal oxidative stress in PCOS rats without affecting the ovarian redox rate. The 16S rDNA sequencing of the intestinal microbiome and non-targeted metabolomics analysis indicated significant differences in gut microbiota composition and serum metabolite profiles between the control and PCOS rats, and most of these differences were reduced after tempol intervention. Tempol alters the gut microbiome by increasing the abundance of genus Ruminococcus_1 and by decreasing the abundance of Ruminococcus_2, Staphylococcus, Ideonella, and Corynebnacterium genera. Tempol also attenuates the reduction of serum bile acid and Stachyose levels in PCOS rats, and the serum Stachyose level was significantly correlated with the abundance of 15 genera, particularly Ruminococcus_1 and Ruminococcus_2. Moreover, Stachyose administration improved ovarian dysfunction in PCOS rats. Thus, our data indicate that tempol ameliorates PCOS phenotype by reducing intestinal oxidative stress, restoring gut dysbiosis, and modulating the interaction between gut microbiota and host metabolite. Therefore, tempol intervention is a potential therapeutic approach for PCOS.
Stachyose Alleviates Corticosterone-Induced Long-Term Potentiation Impairment via the Gut-Brain Axis
Front Pharmacol 2022 Mar 10;13:799244.PMID:35370743DOI:10.3389/fphar.2022.799244.
Stress can induce learning and memory impairment; corticosterone is often used to study the effects and mechanisms of stress in animal models. Long-term potentiation (LTP) has been widely used for tackling the mechanisms of memory. Liuwei Dihuang decoction-active fraction combination (LW-AFC) can improve stress-induced LTP and cognition impairment; Stachyose is an oligosaccharide in LW-AFC. The effects and mechanisms of Stachyose on stress are unknown. In this study, Stachyose showed protective effects against LTP impairment by corticosterone in vivo only via intragastric administration for 7 consecutive days, but there was little effect even after direct intracerebroventricular injection; the protective effect of Stachyose could be canceled by non-absorbable antibiotics (ATB) which disturbed gut flora. 16S rRNA sequencing, alpha diversity, and principal coordinate analysis (PCoA) revealed that the gut flora in corticosterone-treated mice was disturbed and Stachyose could improve corticosterone-induced gut flora disturbance. Bacteroidetes were decreased and Deferribacteres were increased significantly in corticosterone-treated mice, and Stachyose restored Bacteroidetes and Deferribacteres to the normal level. D-serine, a coactivator of NMDA receptors, plays an important role in synaptic plasticity and cognition. Here, corticosterone had little effect on the content of D-serine and L-serine (the precursor of D-serine), but it reduced the D-serine release-related proteins, Na+-independent alanine-serine-cysteine transporter-1 (ASC-1), and vesicle-associated membrane protein 2 (VAMP2) significantly in hippocampus; Stachyose significantly increased ASC-1 and VAMP2 in corticosterone-treated mice, and ATB blocked Stachyose's effects on ASC-1 and VAMP2. NMDA receptors co-agonists L-serine, D-serine, and glycine significantly improved LTP impairment by corticosterone. These results indicated that Stachyose might indirectly increase D-serine release through the gut-brain axis to improve LTP impairment by corticosterone in the hippocampus in vivo.
Stachyose inhibits vancomycin-resistant Enterococcus colonization and affects gut microbiota in mice
Microb Pathog 2021 Oct;159:105094.PMID:34280500DOI:10.1016/j.micpath.2021.105094.
Vancomycin-resistant Enterococcus (VRE) caused nosocomial infections are rising globally. Multiple measures have been investigated to address this issue, altering gut microbiota through dietary intervention represents one of such effort. Stachyose can promote probiotic growth, which makes it a good candidate for potentially inhibiting VRE infection. This study aimed to determine whether Stachyose inhibits VRE colonization and investigated the involvement of gut microbiota this effect of Stachyose. In VRE-infection experiment, 6-week old female C57/6 J mice pre-treated with vancomycin were infected with 2 × 108 CFU VRE via gavage. These mice then received oral administration of Stachyose or PBS as control for 7days. Two groups of uninfected mice were also received daily gavage of Stachyose or PBS for 7 days to observe the impact of Stachyose treatment on normal mice. Fresh fecal and colon samples were collected, then VRE colonization, gut microbiota and gene expression were respectively assessed using cultivation, 16s rRNA sequencing and RNA-sequencing in two parallel experiment, respectively. In VRE-infected mice, Stachyose treatment significantly reduced VRE colonization on days 9 and 10 post-infection. Stachyose treatment increased the relative abundance of Porphyromonadaceae, Parabacteroides, and Parabacteroides distasonis compared to the PBS-treated infection mice (P < 0.01). Uninfected mice treated with Stachyose showed a significant increase in Lactobacillaceae and Lactobacillus compared to the PBS-treated uninfected mice(P < 0.05). RNA-sequencing results showed that Stachyose treatment in VRE-infected mice increased expression of genes involved in TNF and IL-17 signaling pathways. Stachyose treatment also up-regulated Hsd17b14, Cyp3a44, Arg1, and down-regulated Pnliprp2, Ces1c, Pla2g4c genes involving in metabolic pathway in uninfected mice. In conclusion, Stachyose supplementation can effectively inhibit VRE colonization and probably altering composition of the microbiome, which can in turn result in changes in expression of genes. Stachyose may also benefit health by increasing the abundance of Lactobacillus and expression of genes involving in metabolic pathway in normal mice.
Stachyose-induced apoptosis of Caco-2 cells via the caspase-dependent mitochondrial pathway
Food Funct 2015 Mar;6(3):765-71.PMID:25578308DOI:10.1039/c4fo01017e.
Some studies have shown that Stachyose, as prebiotics, can prevent indirectly colon cancer cell growth by promoting the proliferation of probiotics or producing beneficial materials in the intestine. However, its direct inhibitory effects on cancer cells are still unclear. Thus, this study aims to investigate the direct inhibitory effect of Stachyose on human colon cancer cells and determine the molecular mechanism underlying this effect. The MTT assay was used to assess the inhibitory effect of Stachyose on Caco-2 cells. Apoptosis and mitochondrial membrane potential (ΔΨm) measurements were analyzed using flow cytometry. The activities and mRNA expressions of caspases 3 and 9 were determined using caspase assay kits and quantitative real-time polymerase chain reaction. The apoptotic protein expressions of Bcl-2, Bax, and cytochrome C (Cyt C) were detected through western blotting. Results showed that Stachyose inhibits Caco-2 cell proliferation and induces apoptosis in a dose-dependent manner. After pretreatment with 0.4, 0.8, 1.6 and 3.2 mg mL(-1) Stachyose, cell inhibitory rates of 15.31% ± 3.20%, 28.45% ± 2.10%, 40.23% ± 5.70%, and 55.67% ± 4.50% were respectively obtained. Compared with the control, decreases in ΔΨm, increases in caspase 3 and 9 activities and mRNA expressions, down-regulation of Bcl-2 protein expression, up-regulation of the Bax protein and Cyt C release of Caco-2 cells were clearly observed upon exposure to different Stachyose concentrations. The inhibitory mechanism of Stachyose on Caco-2 cells involves the caspase-dependent mitochondrial apoptosis pathway.