Glycosylation of oyster peptides by COS ameliorates zinc deficiency-induced syndromes: intestinal inflammation and imbalance of the gut microbiota in vivo.

Abstract

Zinc is essential for maintaining the integrity and repair of small intestinal epithelial cells while zinc deficiency could induce the inflammatory infiltration and imbalance of intestinal flora in the intestine. In this study, glycosylation between oyster protein hydrolysate (OPH) and chitosan oligosaccharide (COS) was conducted and used as the carrier of zinc ions (OCZn). The results of zeta potential and particle size distribution showed that the OPH-COS successfully bound to zinc ions to form OCZn with a surface zinc content of 0.56% (scanning electron microscopy). In addition, OCZn was found to exhibit good intestinal digestion by in vitro simulated digestion microscopy, while TSQ fluorescence staining revealed the presence of free zinc ions released from OCZn in the intestinal cells. In the zinc deficiency-induced mouse model, a moderate dose of OCZn (zinc: 6.96 mg kg^-1) showed significant restorative effects on colonic inflammation (IL-1β: 28.20 pg per mg·protein, IL-6: 27.73 pg per mg·protein), protein expressions of HO-1 and ZO-1, oxidative stress (the liver and kidneys), and imbalance of the gut microbiota, increasing microbial diversity and abundance (ratio of Firmicutes/Bacteroides). Zinc deficiency triggered the abundance of Proteobacteria (risk of diseases), while the dominant bacteria were mainly restored to Bacteroides, Parabacteroides, Alistipes, Alloprevotella, and Muribaculaceae following the administration of OCZn. This study provided a theoretical basis for improving the inflammatory infiltration of the colon and the imbalance of intestinal flora caused by zinc deficiency.