Citrus pectin protects mice from burn injury by modulating intestinal microbiota, GLP-1 secretion and immune response.

Water-soluble rhamnogalacturonan-I enriched citrus pectin (WRP) has promising effect on antimicrobial defense. We aim to determine whether the modified acidic (A) or neutral (B) WRP solutions can improve intestinal microbial dysbiosis in burn-injured mice. Male Balb/c mice were gavaged with WRPs at 80, 160, 320 mg/kg. Body weight daily for 21 days before exposed to thermal injury of 15 % total body surface area and mortality was monitored. Mice with 80 mg/kg WRPs were also subjected to fecal DNAs and T cell metabonomics analysis, intestinal and plasma glucagon-like peptide 1 (GLP-1) detection, plasma defensin, immunoglobin and intestinal barrier examinations at 1 and 3d postburn (p.b.). Burn-induced mortality was only improved by low dose WRP-A (P = 0.039). Both WRPs could prevent the dysbiosis of gut microbiota in burn injury by reducing the expansion of inflammation-promoting bacteria. Both WRPs suppressed ileum GLP-1 production at 1d p.b. (P = 0.002) and plasma GLP-1 levels at 3d p.b. (P = 0.013). Plasma GLP-1 level correlated closely with ileum GLP-1 production (P = 0.019) but negatively with microbiota diversity at 1d p.b. (P = 0.003). Intestinal T cell number was increased by both WRPs in jejunum at 3d p.b. However, the exaggerated splenic T cell metabolism in burn injury was reversed by both WRPs at 1d p.b. The burn-increased plasma defensin ß1 level was only reduced by WRP-B. Similarly, the intestinal barrier permeability was only rescued by WRP-B at 1d p.b. WRP-A rather than WRP-B could reduce burn-induced mortality in mice by suppressing intestinal GLP-1 secretion, restoring gut microbiota dysbiosis and improving adaptive immune response.

[Influence of Aloe polysaccharide on proliferation and hyaluronic acid and hydroxyproline secretion of human fibroblasts in vitro].

OBJECTIVE: To investigate the effect of Aloe polysaccharide on proliferation and hyaluronic acid and hydroxyproline secretion of human fibroblasts in vitro. METHODS: The fibroblasts were treated with different doses of polysaccharide (0, 25, 50, 100, 200, 400 mg/L). Subsequently, cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, cell cycle by flow cytometry, evaluation of the Aloe polysaccharide toxic effect by acridine orange-ethidium bromide staining, evaluation of the cell injury by lactate dehydrogenase (LDH) assay, and the collagen synthesis by (3)H-proline incorporation. In addition, hyaluronic acid and hydroxyproline levels in the supernatants of cultured fibroblasts were measured by enzyme-linked immunosorbent assay. RESULTS: The proliferation of fibroblasts was induced with polysaccharide in a dose-dependent manner, reaching its highest level on 5th day. Meanwhile, the percentage of cells at phase G(0)/G(1) was decreased, while that at phases G(2)/M and S was increased significantly in Aloe polysaccharide-treated groups as compared with those in the control group (P<0.05). Additionally, the apoptosis of the fibroblasts showed no differences among all groups. The collagen synthesis was increased and cell injury decreased in polysaccharide-treated groups as compared with those in control group (P<0.05), while the levels of hyaluronic acid and hydroxyproline in the supernatants of fibroblasts treated with polysaccharide were significantly higher than those in the control group (P<0.05). CONCLUSION: The Aloe polysaccharide promotes both the proliferation of fibroblasts and the production of hyaluronic acid and hydroxyproline in fibroblasts. This indicates that the Aloe polysaccharide may play an important role in the extracellular matrix remodeling during wound healing.