Peach gum polysaccharides promotes epithelial proliferation to attenuate ulcerative colitis by PI3K/AKT pathway

Peach gum is a homologous substance of medicine and food, mainly composed of polysaccharides. The polysaccharide of peach gum mainly contained 55.5 % of arabinose, 28.1 % of galactose and others. We found PGP could significantly improve symptoms of UC. Further, we found PGP could promote the proliferation of colonic epithelial cells in vivo, and protect the monolayer barrier function formed by Caco2 from LPS damage via PI3K/AKT pathway in vitro. In conclusion, PGP could promote the proliferation of colonic epithelial cells via PI3K/AKT pathway to treat UC. [Display omitted] •Peach gum is a homology of medicine and food, mainly composed of polysaccharides.•PGP could improve symptoms of UC observably in vivo.•PGP activates macrophages and has no direct anti-inflammatory effect in vitro.•PGP could treat UC by promoting colonic epithelial proliferation. Peach gum is a homologous substance of medicine and food, mainly composed of polysaccharides. This study aimed to investigate the effectiveness of Peach gum polysaccharides (PGP) in treatment of ulcerative colitis (UC) and explore its mechanisms. Firstly, we found PGP could decrease the disease activity index, increase length of shortened colon and improve colonic tissue lesions of UC observably in vivo. Further, we explored its mechanisms of anti-UC from aspects of immune regulation and intestinal barrier. On one hand, we found PGP could significantly alleviate inflammation in the colon, but promote the secretion of inflammatory mediators such as IL-6 and TNF-α by RAW264.7 cells in vitro. It is suggested that PGP does not have direct anti-inflammatory effect. On other hand, we found PGP could increase the ki67 protein to promote the proliferation of colonic epithelial cells in vivo and protect the monolayer barrier function formed by Caco-2 from LPS damage via PI3K/AKT pathway in vitro. In conclusion, PGP could promote the proliferation of colonic epithelial cells via PI3K/AKT pathway to treat UC.