Abstract

To investigate the effects of pioglitazone pretreatment on the expression of nuclear factor kappa B and intercellular adhesion molecule-1 and p38 mitogen activated protein kinase pathway in pancreatic tissue of rats with acute pancreatitis. 72 specific pathogen-free adult female Sprague–Dawley rats and male Sprague–Dawley rats were randomly divided into sham operation group, model group and pioglitazone pretreatment group (pretreatment group), with 24 rats in each group. Compared with sham operation group, the amount of ascites in model group was significantly increased, the levels of serum and ascites amylase, serum tumor necrosis factor-alpha, interleukin-6, pancreatic gross score, pancreatic histological score, nuclear factor kappa B and intercellular adhesion molecule-1 in pancreatic tissue were significantly increased. Compared with the model group, the amount of ascites in the pretreatment group was significantly reduced and the levels of serum and ascites amylase, serum tumor necrosis factor-alpha, interleukin-6, pancreatic gross score and pancreatic histological score, the expression levels of nuclear factor kappa B, intercellular adhesion molecule-1 and phospho-p38 mitogen activated protein kinase in pancreatic tissue were significantly decreased (p<0.05). In the sham operation group, the pancreatic tissue structure was clear with occasional inflammatory cells or mild hyperemia and edema and the acinar lobules were intact; in the model group, the pancreatic stroma showed hyperemia and edema, even necrosis, with obvious inflammatory cell infiltration and acinar lobule structure disorder and the pathological changes were gradually aggravated with the extension of time; in the pretreatment group, the pancreatic tissue inflammatory cell infiltration and other pathological changes were observed compared with the model group, it was significantly improved. Pioglitazone pretreatment can inhibit the inflammatory response, reduce the level of amylase, inhibit the expression of nuclear factor kappa B and intercellular adhesion molecule-1 and inhibit the activity of intercellular adhesion molecule-1 signaling pathway in rats with acute pancreatitis.

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