Leonurine Alleviates DSS-Induced Colitis in Mice by Regulating Pancreatic Secretion Pathway and Gut Microbiota.

Abstract

Ulcerative colitis (UC) is a chronic, recurrent inflammatory bowel disease (IBD). Leonurine is an active component in Leonurus japonicus, involved in several processes such as inflammation, oxidation, and other processes. This study found that symptoms of colitis induced by 3% dextran sulfate sodium (DSS) solution in C57BL/6 mice were significantly alleviated after administration of leonurine, in terms of reduced body weight, shortened colon length, disease activity index (DAI), and colonic pathological damage. The expression of the tight junction (TJ) protein claudin-1 and occludin markedly increased, the levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) significantly decreased. Findings from transmission electron microscopy (TEM) and intestinal permeability assessment experiments indicated that leonurine ameliorates the intestinal barrier. Leonurine regulated the pancreatic secretion pathway, significantly reduced the expression levels of Cela2a and Cela3b, and clearly decreased the abundance of Rikenellaceae_RC9_gut_group, UBA1819, Enterococcus, and Oscillibacter. We proposed that leonurine may improve DSS-induced colitis by regulating the pancreatic secretion pathway, modulating the gut microbiota, and improving intestinal barrier, potentially becoming a candidate for the treatment of UC.