Stachyose tetrahydrate

Stachyose Alleviates Corticosterone-Induced Long-Term Potentiation Impairment via the Gut-Brain Axis

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

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.

Tempol ameliorates polycystic ovary syndrome through attenuating intestinal oxidative stress and modulating of gut microbiota composition-serum metabolites interaction

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 triggers apoptotic like cell death in drought sensitive but not resilient plants

Programmed cell death (PCD) is one of the most intensively researched fields in modern mammalian biology with roles in cancer, aging, diabetes and numerous neurodegenerative diseases. It is becoming increasingly clear that PCD also plays significant roles in plant defence and responses to the environment. Given their unique ability to tolerate desiccation (cells remain viable even after they've lost 95% of their water), resurrection plants make ideal models to study the regulation of plant PCD pathways. Previously, we showed that the Australian resurrection plant, Tripogon loliiformis, suppresses plant PCD, via trehalose-mediated activation of autophagy pathways, during drying. In the present study, we created a full-length T. loliiformis cDNA library, performed a large-scale Agrobacterium screen for improved salinity tolerance and identified Stachyose synthase (TlStach) as a potential candidate for improving stress tolerance. Tripogon loliiformis shoots accumulate stachyose synthase transcripts and stachyose during drying. Attempts to generate transgenic plants expressing TlStach failed and were consistent with previous reports in mammals that demonstrated stachyose-mediated induction of apoptosis. Using a combination of transcriptomics, metabolomics and cell death assays (TUNNEL and DNA laddering), we investigated whether stachyose induces apoptotic-like cell death in T. loliiformis. We show that stachyose triggers the formation of the hallmarks of plant apoptotic-like cell death in the desiccation sensitive Nicotiana benthamiana but not the resilient T. loliiformis. These findings suggest that T. loliiformis suppresses stachyose-mediated apoptotic-like cell death and provides insights on the role of sugar metabolism and plant PCD pathways. A better understanding of how resilient plants regulate sugar metabolism and PCD pathways may facilitate future targeting of plant metabolic pathways for increased stress tolerance.

Stachyose modulates gut microbiota and alleviates dextran sulfate sodium-induced acute colitis in mice

Background/aim: Ulcerative colitis (UC) has been implicated to imbalanced enteric flora and reduced microbial diversity. Stachyose is a kind of natural prebiotic which favorably modulate the composition of the gut microbiota. The present study aims to investigate the effects of stachyose on inflammatory levels and gut microbiota of acute colitis mice.
Materials and methods: In this study, the mice were randomly divided into four groups: (1) control group; (2) stachyose group; (3) dextran sulfate sodium (DSS) group; (4) stachyose + DSS group. Hemotoxylin and Eosin (H and E) staining was performed for the distal colon to examine the inflammation and tissue damage. The inflammatory cytokines including IL-6, IL-10, IL-17a, and TNF-α in serum were determined by ELISA assay. The differences in the gut microbiota were analyzed by 16S rDNA gene sequencing.
Results: Histological assay showed that the stachyose treatment significantly reduced the lesions of the colon in DSS-induced colitis. And the upregulated inflammatory cytokines induced by DSS were significantly inhibited by stachyose treatment. Additionally, the sequencing analysis showed that the stachyose changed the gut microbiota composition with a higher level of Akkermansia, as well as selectively increasing some probiotics, including Lactobacillus.
Conclusions: Our results suggested that stachyose increased beneficial microbiota and bacterial diversity to alleviate acute colitis in mice, which might be a new promising option to UC patients.