Effect of ecoimmunonutrition supports on maintenance of integrity of intestinal mucosal barrier in severe acute pancreatitis in dogs

Background One of the major causes of death in severe acute pancreatitis （SAP） is severe infection owing to bacterial translocation. Some clinical studies suggested that ecoimmunonutrition （EIN） as a new strategy had better treatment effect on SAP patients. But the experiment studies on the precise mechanism of the effect of EIN were less reported. In this study, we mainly investigated the effects of EIN on bacterial translocation in SAP model of dogs. Methods SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in healthy hybrid dogs. The SAP dogs were supported with either parenteral nutrition （PN） or elemental enteral nutrition （EEN） or EIN. The levels of serum amylase, serum aminotransferase and plasma endotoxin were detected before and after pancreatitis induction. On the 7th day after nutrition supports, peritoneal fluid, mesenteric lymph nodes （MLN）, liver, and pancreas were collected for bacterial culture with standard techniques to observe the incidence of bacterial translocation. Pathology changes of pancreas were analyzed by histopathologic grading and scoring of the severity of pancreas, and the degree of intestinal mucosal damage was assessed by measuring mucosal thickness, villus height, and crypt depth of ileum. Results Compared with PN and EEN, EIN significantly decreased the levels of serum amylase, serum aminotransferase, plasma endotoxin, and the incidence of bacterial translocation. Furthermore, compared with the others, the histology scores of inflammation in pancreas and the ileum injury （ileum mocosa thickness, villus height, and crypt depth） were significantly alleviated by EIN （P〈0.05）. Moreover, concerning liver function, the serum levels of alanine aminotransferase, aspartate aminotransferase and albumin were ameliorating significantly in the EIN group. Conclusion Our results suggested that EIN could maintain the integrity of intestinal mucosal barrier and reducing the incidence of bacterial translocation in SAP dogs. Early EIN was safe and more effective treatment for SAP dogs.

Renshen(Radix Ginseng) polysaccharide promotes repair of the mice intestinal mucosa through regulatory mechanisms based on polyamine and human antigen R

OBJECTIVE: To investigate the mechanism and effect of Renshen(Radix Ginseng) polysaccharide on the migration of intestinal epithelial cell line 6(IEC-6), as well as the repair mechanism of Renshen(Radix Ginseng) polysaccharide on colonic injury induced by dextran sulfate sodium(DSS) in mice. METHODS: Mice were fed 3%(w/v) DSS for 6 d to create colonic lesions. A cell-migration model was created using cell scratching. m RNA expression, protein expression, translation efficiency of m RNA, and nucleoplasmic distribution of human antigen R(Hu R) were determined by real-time reverse transcription-quantitative polymerase chain reaction, western blotting, a dual luciferase reporter system, and immunofluorescence staining, respectively. RESULTS: Renshen(Radix Ginseng) polysaccharide promoted the migration of IEC-6 cells and affected expression of stromal interaction molecule 1(STIM1) and cell division cycle 42(Cdc42) at transcriptional and posttranscriptional levels. CONCLUSIONS: Renshen(Radix Ginseng) polysaccharideinduced repair of intestinal mucosal injury may be mediated by increased cell migration via polyaminebased regulatory mechanisms. In vitro and in vivo experiments suggest that Renshen(Radix Ginseng) polysaccharide-induced post-transcriptional regulation of STIM1 and Cdc42 may be related to differences in the regulation of different target genes by Hu R. Taken together, these data provide a reference for further exploration of the protective effect of Renshen(Radix Ginseng) on the intestinal mucosa.