Acute pancreatitis leads to pancreatic damage followed by subsequent regeneration. The aim of our study was to evaluate the presence of growth factors in the course of spontaneous pancreatic regeneration after ischemia/reperfusion (I/R)-induced pancreatitis. Methods: In rats, I/R was evoked by clamping of splenic artery for 30 min followed by reperfusion. Rats were sacrificed 1, 5, 12 h or 1, 2, 3, 5, 7, 9 or 21 days after removal of vascular clips. Pancreatic blood flow (PBF), plasma lipase, interleukin-1ßb (IL-1ß), interleukin-10, pancreatic cells proliferation and morphological signs of pancreatitis were determined. Pancreatic presence of fibroblast growth factor-2 (FGF-2), vascular endothelial growth factor (VEGF), platelet-derived growth factor-alpha (PDGF-A) and transforming growth factor-ß type II receptor (TGF-ß RII) was detected by immunohistochemisty. Results: Exposure to I/R led to the development of acute necrotizing pancreatitis followed by regeneration. Morphological features showed maximal pancreatic damage between the 1st and 2nd day of reperfusion. It was correlated with a maximal increase in plasma lipase, and pro-inflammatory IL-1ß concentration, as well as, a reduction in PBF and pancreatic DNA synthesis. I/R increased FGF-2 content in pancreatic acinar cells between the 12th and 24th h, and between 5th and 9th day of reperfusion. At the 2nd day the presence of FGF-2 in pancreatic acinar cells was reduced. After I/R PDGF-A appeared in pancreatic vessels from the 12th h to 5th day of reperfusion. PDGF-A was not observed in pancreatic acinar cells in the control or in I/R group. In pancreatic ducts, the presence of PDGF-A was reduced between the 1st and 3rd, and between 7th and 9th day of reperfusion. In acinar cells, VEGF content was increased after I/R at the time between the 1st and 24th h, and between 3rd and 7th day of reperfusion. At the 2nd day of reperfusion, VEGF was not detected in the pancreatic acinar cells. Moreover, VEGF was found in the inflammatory infiltration, in the tubular complexes between the 2nd and 5th day, and in granulation tissue at the 9th day of reperfusion. In pancreatic acinar cells, I/R caused an increase in TGFß RII presence between the 5th and 24th h, and between 7th and 9th day of reperfusion. Between the 2nd and 5th day of reperfusion the acinar presence of TGFß RII was reduced. In the pancreatic ducts, the presence of TGFß RII was increased after I/R from the 1st h to 9th day of observation. Four weeks after induction of acute pancreatitis, the pancreatic regeneration was completed and the presence of growth factors tested returned to control value. Conclusions: The presence of FGF, VEGF, PDGF-A and TGFß RII is modified in the course of I/R-induced acute pancreatitis. Maximal content of FGF, VEGF and TGFß RII has been observed in early stage of pancreatic regeneration suggesting the involvement these factors in pancreatic recovery.
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