Altered intestinal microflora and barrier injury in severe acute pancreatitis can be changed by zinc
Abstract
To investigate the effect of zinc (Zn) supplementation on intestinal microflora changes and bacterial
translocation in rats with severe acute pancreatitis (SAP), the rats were divided into the sham surgery (SS), SAP,
SS + Zn, and SAP + Zn groups. Saline (0.1 mL/100g) and 5% sodium taurocholate were injected into the
pancreaticobiliary duct of the rats in the SS and SAP + Zn groups, respectively. Intraperitoneal injection of 5
mg/kg Zn was performed immediately after injecting saline or 5% sodium taurocholate into the rats in both
groups. Serum amylase and Zn levels, plasma endogenous endotoxin, intestinal permeability, and the positive
rate of intestinal bacterial translocation were detected, haematoxylin and eosin (H&E) staining was performed,
and the pancreatic tissue scores were calculated for each group. In addition, immunohistochemical (IHC)
staining was performed to evaluate the expression of IL-1β and TNF-α. Real-time fluorescence quantitative
PCR was used to quantify the gene copy numbers of Escherichia, Bifidobacterium, and Lactobacillus in the cecum.
The levels of amylase and plasma endotoxin in the SAP group were significantly higher than those in the SS and
SS + Zn groups. Intestinal mucosal permeability and intestinal bacterial translocation in the liver, pancreas, and
mesenteric lymph nodes were increased in the SAP group. However, the levels of amylase and plasma
endotoxin were decreased as a result of zinc supplementation in the SAP group. The expression of IL-1β and
TNF-α was also reduced to a greater degree in the SAP + Zn group than in the SAP group. Moreover, alleviated
intestinal mucosal permeability and intestinal bacterial translocation in the liver, pancreas, and mesenteric
lymph nodes were found in the SAP + Zn group. The results of real-time quantitative PCR showed that the
gene copy number of Escherichia increased with time, and the gene copy numbers of Lactobacillus and
Bifidobacterium decreased over time. Zn supplementation prevented the release of TNF-α and IL-1β, alleviated
intestinal permeability and endotoxemia, reduced bacterial translocation, and inhibited changes in pathogenic
intestinal flora in rats with SAP.