Apoptosis of the pancreatic acinar cells and acute pancreatitits

Abstract

This study aimed to investigate the mechanism(s) by which crambene causes apoptosis of pancreatic acinar cells and the mechanism(s) through which induction of apoptosis in pancreatic acinar cells by crambene treatment protects against acute pancreatitis. We demonstrate for the first time, that crambene stimulates apoptosis in pancreatic acinar cells in vitro, including PS externalization, caspases activation, mitochondrial depolarization and cytochrome c release. Moreover, this is the first study to demonstrate that how the clearance of apoptotic cells regulates immune responses in acute pancreatitis. Our data show that the anti-inflammatory effect of the phagocytosis is mediated by the production of pancreatic anti-inflammatory mediators such as IL-10. Besides the anti-inflammatory response of phagocytosis, suppressing levels of pancreatic pro-inflammatory mediators also contributes to crambene mediated-protection against mouse acute pancreatitis. These findings would facilitate efforts to rationally manipulate the apoptotic machinery for therapeutic gain in the clinical management of patients with acute pancreatitis.