The improvement of intestinal dysbiosis and hepatic metabolic dysfunction in dextran sulfate sodium‐induced colitis mice: effects of curcumin

Abstract

AbstractBackground and AimCurcumin may have promising application in the prevention and amelioration of inflammatory bowel disease (IBD). However, the underlying mechanisms underpinning the ability of curcumin to interact with the gut and liver in IBD remains to be defined, which is the exploration aim of this study.MethodsMice with dextran sulfate sodium salt (DSS)‐induced acute colitis were treated either with 100 mg/kg of curcumin or phosphate buffer saline (PBS). Hematoxylin–eosin (HE) staining, 16S rDNA Miseq sequencing, proton nuclear magnetic resonance (1H NMR) spectroscopy, and liquid chromatography–tandem mass spectrometry (LC‐MS/MS) were applied for analysis. Spearman's correlation coefficient (SCC) was utilized to assess the correlation between the modification of intestinal bacteria and hepatic metabolite parameters.ResultsCurcumin supplementation not only prevented further loss of body weight and colon length in IBD mice but also improved diseases activity index (DAI), colonic mucosal injury, and inflammatory infiltration. Meanwhile, curcumin restored the composition of the gut microbiota, significantly increased Akkermansia, Muribaculaceae_unclassified, and Muribaculum, and significantly elevated the concentration of propionate, butyrate, glycine, tryptophan, and betaine in the intestine. For hepatic metabolic disturbances, curcumin intervention altered 14 metabolites, including anthranilic acid and 8‐amino‐7‐oxononanoate while enriching pathways related to the metabolism of bile acids, glucagon, amino acids, biotin, and butanoate. Furthermore, SCC analysis revealed a potential correlation between the upregulation of intestinal probiotics and alterations in liver metabolites.ConclusionThe therapeutic mechanism of curcumin against IBD mice occurs by improving intestinal dysbiosis and liver metabolism disorders, thus contributing to the stabilization of the gut–liver axis.