No abstract

No abstract

A homogeneous polysaccharide fraction (DOP-W3-b) with a high intestinal immunomodulating activity was obtained from the stems of Dendrobium officinale through a bioactivity-guided sequential isolation procedure based on the screening of Peyer's patch-mediated immunomodulating activity. Oral administration experiments of mice showed that DOP-W3-b could effectively regulate intestinal mucosal immune activity by changing intestinal mucosal structures, promoting the secretions of cytokines from Peyer's patches (PPs) and mesenteric lymph nodes (MLNs), and increasing the production of secretory immunoglobulin A (sIgA) in the lamina propria. Structure analysis indicated that DOP-W3-b was composed of mannose and glucose in a molar ratio of 4.5 with a relatively low molecular weight of 1.543 × 10(4) Da, and its repeat unit contained a backbone consisting of β-(1→4)-d-Manp, β-(1→4)-d-Glcp and β-(1→3,6)-d-Manp residues, a branch consisting of β-(1→4)-d-Manp, β-(1→4)-d-Glcp and terminal β-d-Glcp, and O-acetyl groups attached to O-2 of β-(1→4)-d-Manp. These results suggested that DOP-W3-b was a new polysaccharide with an essential potential for modulating body's immune functions.

Glucagon-like peptide-1 (GLP-1) secreted from enteroendocrine L-cells is a pleiotropic hormone with beneficial potential related to islet function, diet control, glucose homeostasis, inflammation relief, and cardiovascular protection. The present study aimed at investigating the effect of Polygonatum cyrtonema polysaccharide (PCP) after structural identification on GLP-1 secretion and the possible mechanism involved in the PCP-stimulated secretion of GLP-1. It was found that GLP-1 secretion was effectively promoted (p < 0.01) by PCP both in rats with oral administration for 5 weeks (13.9 ± 0.3–35.8 ± 0.3 pmol/L) and ileal administration within 2 h (13.6 ± 0.4–34.1 ± 1.1 pmol/L) and in enteroendocrine NCI-H716 cells with direct stimulation within 24 h (2.05 ± 0.3–20.7 ± 0.2 pmol/L). The sweet taste receptor T1R2/T1R3 was identified to be essential for NCI-H716 cells to directly recognize PCP. The intervention experiments showed that PCP-stimulated GLP-1 secretion was significantly depressed (p < 0.01) not only by antibodies, siRNA, and the inhibitor of T1R2/T1R3 but also by an adenylate cyclase inhibitor. These results suggest that PCP stimulates GLP-1 secretion from enteroendocrine cells possibly through activation of the T1R2/T1R3-mediated cAMP signaling pathway.