Polysaccharide from Sparassis latifolia alleviates intestinal barrier dysfunction in mice exposed to lead

• Published in: International journal of biological macromolecules 2023-12, Vol.253 (Pt 8), p.127615, Article 127615
• Main Authors: Cheng, Feier, Qiao, Zening, Liang, Guodong, Li, Jiaxin, Qiao, Yaoyao, Yun, Shaojun, Cao, Jinling, Cheng, Yanfen, Chang, Mingchang, Feng, Cuiping
• Format: Article
• Language: English
• Subjects: Animals; Claudin-1 - metabolism; Inflammation - drug therapy; Inflammation - metabolism; Intestinal barrier dysfunction; Intestinal Mucosa - metabolism; Lead - metabolism; Lead toxicity; Mice; Occludin - genetics; Polysaccharides - metabolism; Polysaccharides - pharmacology; Sparassis latifolia polysaccharide
• ISSN: 0141-8130; 1879-0003; 1879-0003
• DOI: 10.1016/j.ijbiomac.2023.127615

Exposure to lead can have harmful effects on the intestines and gut microbiota, leading to toxicity. This study aimed to explore the protective role of Sparassis latifolia polysaccharide (SLP) in safeguarding the intestinal barrier of Kunming mice exposed to lead. The findings indicated that SLP effectively alleviates intestinal lesions, increases the density of cupped cells in the intestine, and reduces inflammation in both serum and the small intestine. Furthermore, SLP maintains the expression of key genes such as ZO-1, Occludin, Claudin-1, Lyz, Ang4, and ZO-2, as well as proteins like claudin-1 and Occludin-1. Furthermore, SLP positively impacts the diversity and richness of microorganisms in the mouse gut microbiota at both the genus and gate levels. It also increases the levels of short-chain fatty acids (SCFAs), including acetic acid, butyric acid, and propionic acid, to varying degrees. In summary, SLP plays a role in alleviating the impaired small intestinal barrier in lead-exposed mice by modulating the intestinal flora, which is consistent with reduced lead absorption. This modulation enhances the integrity of the intestinal barrier, suppresses inflammation, and facilitates the excretion of lead.