Inflammation driven activation of PI3K/Akt/Sp1 signaling pathway and endogenous H2S production aggravate intestinal injury in severe acute pancreatitis |
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Authors: | TANG Ya LIAO Ri-bin XUE Li-wei LIU Ying |
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Institution: | Department of Gastroenterology, The Second Affiliated Hospital of Guilin Medical University, Guilin 541100, China |
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Abstract: | AIM:To investigate the potential role of endogenous hydrogen sulphide (H2S) in severe acute pancreatitis (SAP). METHODS:A rat model of SAP was used to evaluate the role of H2S on intestinal motility by counting the number of fecal pellets and the effect of H2S on the expression of inflammation-related molecule in intestine was investigated. The colonic muscle cells (CMCs) were treated with plasma of SAP rats, tumor necrosis factor-α (TNF-α) or interleukin-6 (IL-6), and the expression of cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), Sp1 and PI3K/Akt related proteins at mRNA and protein levels were determined by RT-qPCR, Western blot and immunohistochemical staining,respectively. The PI3K inhibitor LY294002 and the siRNA-Sp1 were used to suppress the activity of PI3K/Akt/Sp1 signaling pathway. RESULTS:H2S facilitated an inhibitory effect on the intestinal motility and enhanced the inflammatory responses in SAP (P<0.05). The expression of CSE and CBS in CMCs was significantly increased after treatment with TNF-α or IL-6 (P<0.05). Blockage of the PI3K/Akt/Sp1 signaling pathway remarkably inhibited the synthesis of CSE and CBS in CMCs(P<0.05). CONCLUSION:Inflammation driven activation of PI3K/Akt/Sp1 signaling pathway and endogenous production of H2S play a vital role in the pathogenesis of SAP. |
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Keywords: | Severe acute pancreatitis Hydrogen sulphide Inflammation Intestine PI3K/Akt/Sp1 signaling pathway |
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