α-D-1,3-glucan from Radix Puerariae thomsonii improves NAFLD by regulating the intestinal flora and metabolites.

Radix Puerariae thomsonii, the root of the botanical family Fabaceae species Pueraria montana var. thomsonii (Benth.) MR Almeida, can be used as food or medicine. Polysaccharides are important active constituents of this root. A low molecular weight polysaccharide, RPP-2 having α-D-1,3-glucan as the main chain, was isolated and purified. RPP-2 could promote the growth of probiotics in-vitro. Therefore, the effects of RPP-2 on a high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) C57/BL6J mouse models were investigated. RPP-2 could reduce HFD-induced liver injury by reducing inflammation, glucose metabolism, and steatosis, thereby improving NAFLD. RPP-2 regulated the abundances of intestinal floral genera Flintibacter, Butyricicoccus, and Oscillibacter, and their metabolites Lipopolysaccharide (LPS), bile acids, and short-chain fatty acids (SCFAs), thereby improving inflammation, lipid metabolism, and energy metabolism signaling pathways. These results confirmed that RPP-2 play a prebiotic role by regulating intestinal flora and microbial metabolites, playing a multi-pathway and multi-target role in improving NAFLD.

Radix Puerariae thomsonii polysaccharide (RPP) improves inflammation and lipid peroxidation in alcohol and high-fat diet mice by regulating gut microbiota.

Polysaccharides are the important active constituents of Radix Puerariae thomsonii. Numerous studies have shown that polysaccharides can regulate gut microbiota, repair intestinal barrier, and affect the microbiota-intestine-liver axis, thereby showing therapeutic effects on metabolic disorders. In this study, Radix Puerariae thomsonii polysaccharide (RPP) was extracted from Radix Puerariae thomsonii. The average Mw of RPP was determined to be 1.09 × 105 Da and the monosaccharide composition showed it consisted of glucose. The effects and underlying mechanisms of RPP on fatty liver were studied using C57/BL6J mice induced by alcohol and high-fat diet. The results showed that the oral supplementation of RPP could alleviate alcohol and high-fat diet-induced hepatic injury and steatosis. RPP also promoted intestinal barrier integrity and reduced inflammation through NF-κB signaling pathway. RPP could ameliorate the lipid peroxidation by AMPK/NADPH oxidase signaling pathway. Additionally, these improvements might be related to the enrichment of intestinal bacteria Parabacteroides (promote intestinal barrier integrity) and Prevotellaceae UCG 001 (activation of AMPK signaling pathway). These results demonstrated that RPP could improve inflammation and lipid peroxidation in the alcohol and high-fat diet mouse by restoring the intestinal barrier integrity and regulating the gut microbiota. This suggested that RPP was a potential food supplement for the treatment of fatty liver disease.