Effect of Down-regulated MUC2 Transcription on Intestinal Permeability in Rats With Acute Necrotizing Pancreatitis / 胃肠病学

ABSTRACT

Background:Acute pancreatitis can induce intestinal barrier dysfunction in its early phase,which is closely related with the progression and prognosis of the disease. Intestinal mucus layer not only serves as a physical barrier between pathogens and epithelium,but also plays a critical role in the maintenance of intestinal barrier function. Aims:To investigate the expression and role of mucin 2 (MUC2)in injured intestinal barrier in rats with acute necrotizing pancreatitis (ANP). Methods:Forty-two male Sprague-Dawley rats were randomly divided into two groups:the sham operation (SO)group and ANP group,which were induced via a retrograde injection of 3. 5% sodium taurocholate into biliopancreatic duct. Blood,pancreas and colon samples were obtained 6,12 and 24 hours after establishing the ANP model for determination of serum amylase and D-lactate (an indicator of intestinal permeability)and histopathological examination. PAS/ AB staining was used to observe the colon mucus layer and goblet cells,and the expressions of MUC2 and inflammatory cytokines in colonic tissue were detected by real-time PCR. Results:ANP models were successfully established. In ANP group,obvious colonic injury,increased intestinal permeability,thinner colon mucus layer,reduced mucin-containing goblet cells,down-regulated MUC2 mRNA and up-regulated tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β)and interferon-γ (IFN-γ)mRNAs were observed at each time point as compared with those in SO group (P < 0. 05). Spearman correlation coefficient revealed that MUC2 expression was negatively correlated with the intestinal permeability and expression of inflammatory cytokines in ANP group (P < 0. 05). Conclusions:Transcription of MUC2 is significantly down-regulated in colonic tissue of ANP rats,and might be associated with increased intestinal permeability and excessive expression of inflammatory cytokines in early phase of ANP.