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.

Dynamic Monitoring of Immunoinflammatory Response Identifies Immunoswitching Characteristics of Severe Acute Pancreatitis in Rats

“…It was found that intestinal dilatation, epithelial cell shedding, and inflammatory infiltration occurred at 12 h in SAP rats. The severity of SAP patients is closely related to intestinal mucosa permeability ( 12 , 39 ), and intestinal mucosal permeability is commonly known as the most direct and accurate element that reflects intestinal mucosal barrier function ( 40 , 41 ). D-lactate, which is a kind of the intestinal metabolite, enters the blood circulation and significantly increases when the intestinal mucosal barrier function is seriously damaged ( 42 ).…”

Role of Autophagy Inducers and Inhibitors in Intestinal Barrier Injury Induced by Intestinal Ischemia–Reperfusion (I/R)

“…Subsequently, the intestinal sections were stained with 3,3′-diaminobenzidine (DAB) and hematoxylin. Both HE staining and IHC staining were performed according to the method of Su and Tang [ 20 ].…”

Gut Microbiota as a Mediator of Essential and Toxic Effects of Zinc in the Intestines and Other Tissues

“…Specifically, Zn sulfate supplementation in rats with pancreatitis significantly reduced endotoxic accumulation (LPS) and tissue IL-1β and TNFα expression, as well as attenuated pancreatitis-associated gut permeability and bacterial translocation to pancreas, liver, and mesenterial lymph nodes. The impact of Zn on gut microflora biodiversity was characterized by a reduction in Escherichia numbers, and an elevation of Bifidobacterium and Lactobacillus gene copy numbers in caecum [ 74 ]. Correspondingly, in patients with chronic pancreatitis characterized by high incidence (~40%) of small intestinal bacterial overgrowth, the latter was characterized by a significant negative correlation with serum Zn levels [ 75 ].…”