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AIM:To investigate the effect of emodin on pancreatic claudin-5 and occludin expression,and pancreatic paracellular permeability in acute pancreatitis(AP).METHODS:Experimental pancreatitis was induced by retrograde injection of 5% sodium taurocholate into the biliopancreatic duct.Emodin was injected via the external jugular vein 0 or 6 h after induction of AP.Rats from sham operation and AP groups were injected with normal saline at the same time.Samples of pancreas were obtained 6 or 12 h after drug administration.Pancreatic morphology was examined with hematoxylin and eosin staining.Pancreatic edema was estimated by measuring tissue water content.Tumor necrosis factor(TNF)-α and interleukin(IL)-6 level were measured by enzyme-linked immunosorbent assay.Pancreatic paracellular permeability was assessed by tissue dye extravasation.Expression of pancreatic claudin-5 and occludin was examined by immunohistology,quantitative real-time reverse transcriptase polymerase chain reaction and western blotting.RESULTS:Pancreatic TNF-α and IL-6 levels,wet/dry ratio,dye extravasation,and histological score were significantly elevated at 3,6 and 12 h following sodium taurocholate infusion;treatment with emodin prevented these changes at all time points.Immunostaining of claudin-5 and occludin was detected in rat pancreas,which was distributed in pancreatic acinar cells,ductal cells and vascular endothelial cells,respectively.Sodium taurocholate infusion significantly decreased pancreatic claudin-5 and occludin mRNA and protein levels at 3,6 and 12 h,and that could be promoted by intravenous administration of emodin at all time points.CONCLUSION:These results demonstrate that emodin could promote pancreatic claudin-5 and occludin expression,and reduce pancreatic paracellular permeability.
AIM: To investigate the effect of emodin on pancreatic claudin-5 and occludin expression, and pancreatic paracellular permeability in acute pancreatitis (AP). METHODS: Experimental pancreatitis was induced by retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. Emodin was injected via the external jugular vein 0 or 6 h after induction of AP. Rats from sham operation and AP groups were injected with normal saline at the same time. Samples of pancreas were obtained 6 or 12 h after drug administration. Pancreatic morphology was examined with hematoxylin and eosin staining. Pancreatic edema was estimated by measuring tissue water content. Tumor necrosis factor (TNF) -α and interleukin (IL) -6 level were measured by enzyme-linked immunosorbent assay. Pancreatic paracellular permeability was assessed by tissue dye extravasation. Expression of pancreatic claudin-5 and occludin was examined by immunohistology, quantitative real-time reverse transcriptase polymerase chain reaction and w estern blotting.RESULTS: Pancreatic TNF-α and IL-6 levels, wet / dry ratio, dye extravasation, and histological score were significantly elevated at 3, 6 and 12 h following sodium taurocholate infusion; treatment with emodin prevented these changes at all time points. Immunostaining of claudin-5 and occludin was detected in rat pancreas, which was distributed in pancreatic acinar cells, ductal cells and vascular endothelial cells, respectively. Sodium taurocholate infusion was significantly decreased pancreatic claudin-5 and occludin mRNA and protein levels at 3, 6 and 12 h, and that could be promoted by intravenous administration of emodin at all time points. CONCLUSION: These results demonstrate that emodin could promote pancreatic claudin-5 and occludin expression, and reduce pancreatic paracellular permeability.