In the process of
ischemia-reperfusion injury, intestinal
ischemia and
inflammation interweave, leading to tissue damage or
necrosis. However,
oxygen radicals and inflammatory mediators produced after reperfusion cause tissue damage again, resulting in severe intestinal epithelial barrier dysfunction. The aim of this study was to determine the protective effect of
somatostatin on intestinal epithelial barrier function during intestinal
ischemia-reperfusion injury and explore its mechanism. By establishing a rat intestinal
ischemia-reperfusion model, pretreating the rats with
somatostatin, and then detecting the histopathological changes, intestinal permeability and expression of
tight junction proteins in intestinal tissues, the protective effect of
somatostatin on the intestinal epithelial barrier was measured in vivo. The mechanism was determined in
interferon γ (IFN-γ)-treated Caco-2 cells in vitro. The results showed that
somatostatin could ameliorate
ischemia-reperfusion-induced intestinal epithelial barrier dysfunction and protect Caco-2 cells against IFN-γ-induced decreases in
tight junction protein expression and increases in monolayer cell permeability. The expression of Tollip was upregulated by
somatostatin both in
ischemia-reperfusion rats and IFN-γ-treated Caco-2 cells, while the activation of TLR2/MyD88/NF-κB signaling was inhibited by
somatostatin. Tollip inhibition reversed the protective effect of
somatostatin on the intestinal epithelial barrier. In conclusion,
somatostatin could attenuate
ischemia-reperfusion-induced intestinal epithelial barrier injury by inhibiting the activation of TLR2/MyD88/NF-κB signaling through upregulation of Tollip.