Effects and mechanisms of somatostatin analogs on apoptosis of pancreatic acinar cells in acute pancreatitis in mice

Abstract Aim: To investigate the effects of somatostatin analogs (SSa) on apoptosis of pancreatic acinar cells and apoptosis‐regulated gene bax , and p53 in treating acute pancreatitis in mice. Methods: In cerulein‐induced pancreatitis, with or without treatment of somatostatin, analogs (Octreotide) in CD‐1 (BALB/c × DΒΑ/1) mice, apoptosis of pancreatic acinar cells was detected by using the TdT‐mediated dUTP nick‐end labeling (TUNEL) method, and the expression of apoptosis‐regulated gene bax and p53 was determined by using the streptavidin‐peroxidase immunohistochemical technique and the RT‐PCR method, respectively. Results: On HE staining, acinar cells in the pancreas showed pyknotic nuclei and the formation of apoptotic bodies, which are the typical morphological features of apoptosis. Regarding TUNEL use, the apoptotic index of pancreatic acinar cells in the non‐treated group at 5 and 14 h after induction of acute pancreatitis was significantly lower than those of the SSa‐treated group, respectively ( P < 0.01). On immunohistochemistry and RT‐PCR, there was an expression of neither bax nor p53 in normal pancreatic tissues. The expression of bax in the SSa‐treated group at 5 and 14 h after treatment of SSa was markedly higher than those of the non‐treated group, respectively ( P < 0.01), but there was no significant difference in the expression of p53 between the SSa‐treated group and the non‐treated group. Conclusions: The induction of apoptosis in pancreatic acinar cells injury to reduce inflammatory reaction might be one of the mechanisms of SSa in treating acute pancreatitis in mice, and the mechanisms of apoptosis probably correlated with the expression of apoptosis‐regulated gene bax , but have no relationship with the expression of p53 .