Sulfated Chinese Yam Polysaccharides Alleviate LPS-Induced Acute Inflammation in Mice through Modulating Intestinal Microbiota.

This study aimed to test the preventive anti-inflammatory properties of Chinese yam polysaccharides (CYP) and sulfated Chinese yam polysaccharides (SCYP) on LPS-induced systemic acute inflammation in mice and investigate their mechanisms of action. The results showed that SCYP can efficiently reduce plasma TNF-α and IL-6 levels, exhibiting an obvious anti-inflammation ability. Moreover, SCYP reduced hepatic TNF-α, IL-6, and IL-1ß secretion more effectively than CYP, and significantly altered intestinal oxidative stress levels. In addition, a 16S rRNA gene sequencing analysis showed that CYP regulated the gut microbiota by decreasing Desulfovibrio and Sutterella and increasing Prevotella. SCYP changed the gut microbiota by decreasing Desulfovibrio and increasing Coprococcus, which reversed the microbiota dysbiosis caused by LPS. Linear discriminant analysis (LDA) effect size (LEfSe) revealed that treatment with CYP and SCYP can produce more biomarkers of the gut microbiome that can promote the proliferation of polysaccharide-degrading bacteria and facilitate the intestinal de-utilization of polysaccharides. These results suggest that SCYP can differentially regulate intestinal flora, and that they exhibit anti-inflammatory effects, thus providing a new reference to rationalize the exploitation of sulfated yam polysaccharides.

The Molecular Mechanism of Yam Polysaccharide Protected H2O2-Induced Oxidative Damage in IEC-6 Cells.

Oxidative stress is involved in maintaining homeostasis of the body, and an in-depth study of its mechanism of action is beneficial for the prevention of chronic illnesses. This study aimed to investigate the protective mechanism of yam polysaccharide (CYP) against H2O2-induced oxidative damage by an RNA-seq technique. The expression of genes and the function of the genome in the process of oxidative damage by H2O2 in IEC-6 cells were explored through transcriptomic analysis. The results illustrated that H2O2 damaged cells by promoting cell differentiation and affecting tight junction proteins, and CYP could achieve cell protection via restraining the activation of the MAPK signaling pathway. RNA-seq analysis revealed that H2O2 may damage cells by promoting the IL-17 signaling pathway and the MAPK signaling pathway and so forth. The Western blot showed that the pretreatment of CYP could restrain the activation of the MAPK signaling pathway. In summary, this study demonstrates that the efficacy of CYP in modulating the MAPK signaling pathway against excessive oxidative stress, with a corresponding preventive role against injury to the intestinal barrier. It provides a new perspective for the understanding of the preventive role of CYP on intestinal damage. These findings suggest that CYP could be used as oxidation protectant and may have potential application prospects in the food and pharmaceutical industries.