Abstract
Polysaccharides from Panax ginseng C. A. Meyer (P. ginseng) are the main active component of P. ginseng and exhibit significant intestinal anti-inflammatory activity. However, the therapeutic mechanism of the ginseng polysaccharide is unclear, and this hinders the application for medicine or functional food. In this study, a polysaccharide was isolated from P. ginseng (GP). The primary structure and morphology of the GP were studied by HPLC, FT-IR spectroscopy, and scanning electron microscopy (SEM). Further, its intestinal anti-inflammatory activity and its mechanism of function were evaluated in experimental systems using DSS-induced rats, fecal microbiota transplantation (FMT), and LPS-stimulated HT-29 cells. Results showed that GP modulated the structure of gut microbiota and restored mTOR-dependent autophagic dysfunction. Consequently, active autophagy suppressed inflammation through the inhibition of NF-κB, oxidative stress, and the release of cytokines. Therefore, our research provides a rationale for future investigations into the relationship between microbiota and autophagy and revealed the therapeutic potential of GP for inflammatory bowel disease.
Highlights
Inflammatory bowel disease (IBD) consists of a group of disorders including Crohn’s disease (CD) and ulcerative colitis (UC) and is a kind of recurrent, refractory gastrointestinal disease [1]
HPLC results showed that ginseng polysaccharide (GP) was composed of galacturonic acid (GalA), glucose (Glc), galactose (Gal), and arabinose (Ara) in a molar ratio of 1.6 to 5.1 to 1.0 to 1.6, respectively (Figure 1B)
Corroborating the above data and the previous reports [32, 39], we demonstrated that the increased levels of LPS were associated with the rising abundance of Gram-negative bacteria in the intestines of the dextran sodium sulphate (DSS)-induced model rats and that GP could regulate the structure of gut microbiota and reduce the abundance of Gram-negative bacteria that produce LPS
Summary
Inflammatory bowel disease (IBD) consists of a group of disorders including Crohn’s disease (CD) and ulcerative colitis (UC) and is a kind of recurrent, refractory gastrointestinal disease [1]. Inflammatory infiltration, redox imbalance, and gut microbiota dysbiosis are involved in the initiation, development, and exacerbation of intestinal inflammatory diseases. Intestinal epithelium plays an important role in maintaining gut homeostasis and is the main defense against pathogen invasion [2]. It has been reported that the regulation of gut microbiota can alleviate the inflammatory response induced by dextran sodium sulphate (DSS) in mice. Lipopolysaccharide (LPS) is the main component of the cell walls of many
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