Abstract

Objective to investigate the expression of NF-κB and occludin in intestinal mucosal barrier during severe acute pancreatitis (SAP) and its clinical significance. Method Twenty-four Wistar rats were randomly divided into a normal control group, an SAP group, and a PDTC group. The rats were sacrificed at 24h after modeling, and general appearance of the abdominal cavity, pathological changes of the intestinal mucosa, changes in intestinal mucosal permeability were observed, serum inflammatory factor IL-1 was measured, and expression of tight junction protein occludin in the intestinal epithelial cells were determined by immunohistochemistry. Results Rats of the SAP group showed obvious inflammatory reaction in the abdominal cavity, manifested by enlargement of intestinal tract, intestinal edema, and increased permeability of intestinal barrier, whereas NF-κB inhibitor alleviated intestinal damage and intestinal mucosa edema, upregulated intestinal epithelial tight junction protein occludin, decreased intestinal permeability, and lowered the level of inflammatory factors. Conclusion Impairment of intestinal barrier function during SAP may be associated with increased NF-κB and decreased intestinal tight junction protein occludin; inhibiting NF-kB may alleviate intestinal mucosal barrier dysfunction during SAP.

Highlights

  • Severe acute pancreatitis (SAP) is a common severe clinical situation

  • 71 Qingyun Zhu et al.: Expression of NF-κB and Occludin in Intestinal Mucosal Barrier During Severe Acute Pancreatitis and Its Clinical Significance pyrrolidine dithiocarbamate (PDTC), FITC-labeled dextran 4000 (FD 4) were purchased from Sigma; ELISA kit, anti-occludin goat polyclonal antibody (IgG) was purchased from Santa Cruz Biotechnology; immunohistochemistry kit, DAB staining kit, and anti-off slides were purchased from Fuzhou Maixin biotechnology

  • No damage to the intestinal mucosa was observed in the control group, while intestinal mucosal destruction was observed in the SAP and PDTC group

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Summary

Introduction

Severe acute pancreatitis (SAP) is a common severe clinical situation. This disease is manifested by structural and functional abnormalities of the intestinal epithelial tight junction and leads to increased intestinal mucosal permeability, increased translocation of intestinal bacteria and toxins, and secondary systemic infection and inflammatory response, which makes SAP a major cause of sepsis. Studies have shown that the major causes of intestinal mucosal barrier dysfunction, increased intestinal permeability, and intestine-derived infection are several cytokines and inflammatory mediators. We constructed a rat model of SAP, and observed the effect of specific NF-κB blocker on intestinal mucosal barrier function. Expression of tight junction protein occludin was determined to clarify the mechanism how NF-κB affect intestinal mucosal barrier impairment in SAP rats

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