Probiotic-fermented black tartary buckwheat alleviates hyperlipidemia and gut microbiota dysbiosis in rats fed with a high-fat diet.

Natural plants fermented with probiotics exert beneficial effects on hyperlipidemia and gut microbiota disorders. This study aimed to investigate the hypolipidemic activity of fermented black tartary buckwheat (FBTB) in rats with hyperlipidemia induced by a high-fat diet (HFD) in association with the regulation of gut microbiota. Probiotic fermentation by Bacillus sp. DU-106 obviously increased the contents of tyrosine, lysine, total flavonoids, total polyphenols, quercetin, and kaempferol in black tartary buckwheat (BTB) and significantly decreased the rutin content. FBTB treatment for 8 weeks significantly decreased the levels of serum total cholesterol, triglycerides, and low-density lipoprotein cholesterol in HFD-induced hyperlipidemic rats. Western blot analysis further confirmed that the protein expression levels of FXR, SREBP1, and PPARα were altered after FBTB treatment. Moreover, FBTB intervention altered the gut microbiota of HFD-fed rats by increasing the relative abundances of Lactobacillus, Faecalibaculum, and Allobaculum and decreasing the relative abundance of Romboutsia. The relative abundance of Allobaculum was positively correlated with the levels of tyrosine, total flavonoids, total polyphenols, quercetin and kaempferol and negatively correlated with that of rutin. These results suggested that FBTB could alleviate hyperlipidemia and gut microbiota dysbiosis in HFD-fed rats.

Supplementation of Bacillus sp. DU-106 reduces hypercholesterolemia and ameliorates gut dysbiosis in high-fat diet rats.

Gut microbiota modulation by a probiotic is a novel therapy for hypercholesterolemia mitigation. This study initially investigated the potential hypocholesterolemic effect of Bacillus sp. DU-106 in hypercholesterolemic rats and explored its potential relation with gut microbiota. Sprague-Dawley rats received a high-fat diet, or a high-fat diet supplemented with 7.5 × 109 and 1.5 × 1010 CFU/kg bw/day Bacillus sp. DU-106 (low-dose and high-dose groups). At the end of 9 weeks, Bacillus sp. DU-106 treatment significantly decreased the body weight, liver index, and total cholesterol. 16S rRNA sequencing showed that Bacillus sp. DU-106 intervention significantly increased bacterial richness and particularly increased the genus abundance of Turicibacter, Acinetobacter, Brevundimonas, and Bacillus and significantly decreased the abundance of Ralstonia. Metabolomic data further indicated that the supplementation of Bacillus sp. DU-106 remarkably changed the gut metabolic profiles of hypercholesterolemic rats and, in particular, elevated the metabolites of indole-3-acetate, methylsuccinic acid, creatine, glutamic acid, threonine, lysine, ascorbic acid, and pyridoxamine. Spearman's correlation analysis showed the close relation between the different genera and metabolites. In conclusion, Bacillus sp. DU-106 supplement ameliorated high-fat diet-induced hypercholesterolemia and showed potential probiotic benefits for the intestine. KEY POINTS: • A novel potential probiotic Bacillus sp. DU-106 ameliorated hypercholesterolemia in rats. • Bacillus sp. DU-106 supplement regulated gut microbiome structure and richness. • Bacillus sp. DU-106 supplement changed metabolic profiles in high-fat diet rats. • Significant correlations were observed between differential genera and metabolites.

Structural characteristics of a mannoglucan isolated from Chinese yam and its treatment effects against gut microbiota dysbiosis and DSS-induced colitis in mice.

A water-soluble polysaccharide named CYP-1 was isolated from Chinese yam. CYP-1 was characterized as a mannoglucan having a backbone consisting predominately of 1,4-α-linked Glcp branched at O-2, O-3, and O-6 position by t-α-linked Manp with a molecular weight of 2.86 kDa. CYP-1 could inhibit the overproduction of pro-inflammatory cytokines (such as TNF-α and IL-1ß) in LPS-induced RAW 264.7 cells and DSS-induced colitis mice. Oral administration of CYP-1 dramatically alleviated colonic pathological damage, suppressed the activation of colonic inflammatory signaling pathways (such as NF-κB and NLRP3 inflammasome), recovered the mRNA expression of junctional proteins (such as ZO-1, claudin-1, occludin, and connexin-43), and modulated the gut microbiota by decreasing the abundances of Alistipes, Helicobacter, and an unidentified Enterobacteriaceae, in DSS-induced colitis mice. Overall, the present study elucidated that a new polysaccharide structure CYP-1 from Chinese yam and its therapeutic potential as a prebiotic for the prevention of inflammatory bowel disease.

Sacha inchi oil alleviates gut microbiota dysbiosis and improves hepatic lipid dysmetabolism in high-fat diet-fed rats.

Dietary ω-3 polyunsaturated fatty acids (PUFAs) are beneficial for humans against the development of hyperlipidaemia, but the underlying mechanisms are still poorly understood. Here, we demonstrated that oral consumption of sacha inchi oil, which is rich in α-linolenic acid, alleviated dyslipidemia, hepatic steatosis and inflammatory infiltration in high-fat diet (HFD)-fed rats. Sacha inchi oil administration reversed gut microbiota dysbiosis and altered the gut microbiota metabolome and in particular prevented bile acid dysmetabolism caused by a HFD. Sacha inchi oil intake ameliorated hepatic lipid dysmetabolism in HFD-fed rats, via potentiating the biosynthesis and reuptake of bile acids, reducing the de novo lipogenesis, promoting fatty acid beta-oxidation, and alleviating the dysregulation of glycerolipid, glycerophospholipid, and sphingolipid metabolisms. The results showed that dietary sacha inchi oil can alleviate gut microbiota dysbiosis and reduce lipid dysmetabolism in HFD rats, and provide novel insights into the molecular mechanisms by which plant-derived ω-3 PUFAs prevent the development of hyperlipidaemia.

Anticancer Action of Psilostachyin-A in 5-Fluorouracil-Resistant Human Liver Carcinoma are Mediated Through Autophagy Induction, G2/M Phase Cell Cycle Arrest and Inhibiting Extracellular-Signal-Regulated Kinase/Mitogen Activated Protein Kinase (ERK/MAPK) Signaling Pathway.

BACKGROUND Liver cancer is one of the most common malignancies around the world and one of the major causes of cancer related mortality. The objective of this study was to evaluate the anticancer effect of the natural compound psilostachyin-A on 5-fluorouracil-resistant human liver carcinoma cells and its effects on autophagy, cell cycle, caspase activation, and the ERK/MAPK signaling pathway. MATERIAL AND METHODS Cell Counting Kit 8 (CCK-8) assay was used to evaluate the effects on HepG2 cell viability at different doses of psilostachyin-A. Cell cycle analysis was performed using flow cytometry, and Transwell assay was used to check effects on cell invasion. Transmission electron microscopic studies were done to evaluate autophagy induced by psilostachyin-A, and the western blot method was carried out to evaluate the effects on autophagy and the ERK/MAPK signaling pathway. RESULTS CCK-8 assay revealed that the psilostachyin-A reduced the cell viability of HepG2 cancer cells in a dose dependent manner. Psilostachyin-A also reduced the colony forming potential of HepG2 cells, concentration dependently. The IC50 of psilostachyin was found to be 25 µM. The anticancer effects of psilostachyin-A were due to the induction of autophagy which was accompanied by enhancement of LC3B II expression. Psilostachyin also caused cell cycle arrest by enhancing the accumulation of HepG2 cells in the G2/M phase. Transwell assay showed that psilostachyin-A suppressed the invasion of HepG2 cells. The results also showed that psilostachyin-A could block the ERK/MAPK pathway, indicative of the cytotoxic effects of psilostachyin-A on liver cancer. CONCLUSIONS These preliminary observations suggested that psilostachyin-A might prove beneficial in the treatment of liver cancer.