LAUSR

Background Intestinal injury caused by severe acute pancreatitis (SAP) can induce peripancreatic and systemic infection, and aggravate systemic inflammation. Emodin has demonstrated efficacy in mitigating SAP-associated intestinal injury. Although metabolites in tissues cause histopathophysiological changes, data on the mechanisms of emodin on metabolic processes remain scant. Methods The SAP-related intestinal injury rat model was induced by injection of 3.5% sodium taurocholate solution through the biliopancreatic duct. The protective effect of emodin on intestinal injury was evaluated by histologic analyses. On the other hand, we assessed the effect of emodin on metabolic remodeling in intestinal tissues using untargeted metabolomics. Results Out of the analyzed 1187 metabolites, untargeted metabolomics identified 99 differential metabolites in the intestinal tissues. Emodin significantly alleviated the inflammatory injury in the pancreas and intestines. Emodin treatment led to significant changes in bile acid metabolism, amino acid metabolism, intestinal microbiota related metabolism, and glycerol phospholipid metabolism in the intestinal tissues. In addition, using the weighted gene co-expression network analysis, we constructed emodin related metabolite–metabolite interaction network and showed that intestinal microbiota related metabolites and glycerol phospholipid metabolism were associated with emodin treatment. Glycine, LPC (0:0/22:6), Spermidine, 11β-hydroxyprogesterone, and N1-methyl-2-Pyridone-5-carboxamide may be efficient molecules after emodin treatment. Conclusion Taken together, our data demonstrated that intestinal injury caused by SAP induces an obvious metabolic disorder. Emodin exerts its therapeutic effects through metabolic remodeling.