The intestinal inflammation caused by intestinal ischemia reperfusion during acute pancreatitis (AP) often leads to multiple
organ dysfunction and aggravation of acute pancreatitis. This review concerns up-date progress of the pathophysiology and molecular
mechanism of the excessive production of gut-derived cytokines. The regulation effects of immuno-neuro-endocrine network for pancreatic
necrosis are the basis for pharmacological therapeutic in AP. The translation from basic research to clinical trials for the prevention
or treatment of severe acute pancreatitis (SAP) is of great value. Early enteral nutrition is necessary for the restitution, proliferation, and
differentiation of the intestinal epithelial cells adjacent to the wounded area. Clearance of the excess intestinal bacteria and supplement of
probiotics may be helpful to prevent bacterial translocation and infection of pancreas.
Keywords: Acute pancreatitis, intestinal inflammation, intestinal ischemia reperfusion, intestinal barrier, intestinal bacteria, cytokines, somatostatin,
tumor necrosis factor-α, melatonin, intestinal restitution, enteral nutrition.
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