Pine Pollen Polysaccharides’ and Sulfated Polysaccharides’ Effects on UC Mice through Modulation of Cell Tight Junctions and RIPK3-Dependent Necroptosis Pathways

Abstract

The purpose of this study is to explore the effects of pine pollen polysaccharides and sulfated polysaccharides on mice with ulcerative colitis and whether they could protect mice from inflammation by regulating the tight junctions of colonic epithelial cells and regulating the RIPK3-dependent necroptosis pathways. Pine pollen polysaccharides were prepared by water boiling and ethanol precipitation. After deproteinedization with trichloroacetic acid, the UV spectrum showed that there were no proteins. One polysaccharide component (PPM60-III) was made by gel filtration chromatography, and then sulfated polysaccharide (SPPM60-III) was derived using the chlorosulfonic acid-pyridine method. After treatment with PPM60-III and SPPM60-III, the body weight of mice with ulcerative colitis induced by dextran sodium sulfate increased, the DAI score decreased, the levels of pro-inflammatory factors and inflammation-related enzymes decreased, and the level of anti-inflammatory factors increased. In addition, after treatment, the expressions levels of tight junction proteins increased, the expressions levels of key proteins of programmed necroptosis decreased, while the level of Caspase-8 increased. The results indicated that pine pollen polysaccharides and sulfated polysaccharides have a certain therapeutic effect on UC mice, and the therapeutic effect may be achieved by regulating the tight junction of colonic epithelial cells and regulating the RIPK3-dependent necroptosis pathways

Polysaccharide from Smilax glabra Roxb Mitigates Intestinal Mucosal Damage by Therapeutically Restoring the Interactions between Gut Microbiota and Innate Immune Functions

“…Thus, therapeutic renovation of epithelial barrier function may play a crucial role in addressing the symptoms of UC. According to previous reports, polysaccharides reduce TJ disintegration and apoptosis in the colon epithelium of mice with DSS-induced colitis [49,50]. Likewise, in the current study, the downregulated tissue levels of TJ proteins, including ZO-1, occludin, claudin loss off microscopic AJ, TJ, DS, and the microvilli that constitute the brush border in DSS-induced colitis mice, were considerably improved by SGPs.…”

Galangin modulation of the IL-23/IL-17 axis mitigates ulcerative colitis through attenuation of oxidative/nitrative stress and inflammation

“…A 10-year illness course is experienced by around one-third of UC patients. Since UC has already spread globally, finding new and powerful medications to treat UC remains a key objective [3,13,14]. Galangin (Gal; 3,5,7-trihydroxyflavone), a natural flavonoid compound derived from the rhizome of Alpinia officinarum, has gained considerable attention due to its potential therapeutic properties.…”