LIPOPOLYSACCHARIDE-INDUCED APOPTOSIS OF RAT PANCREATIC ACINAR-CELLS

Background-Bacterial lipopolysaccharide (LPS) has been proposed to par ticipate in the pathogenesis of pancreatic inflammatory disease. Aims- This study investigated the role of endotoxaemia in the pathogenesis o f pancreatic acinar cell injury. Methods-Sixty eight male Spraque-Dawl ey rats were used in the study. Escherichia coli LPS (5 mg/kg) was inj ected into the peritoneal cavity of the rats. The concentration of pan creatic phospholipase A(2) (PLA(2)) in plasma was measured and pancrea tic tissue examined by histology, in situ detection of free DNA 3'-end s, and electrophoretic DNA analysis. Results-The concentration of panc reatic PLA(2) increased in plasma and the catalytic activity of PLA(2) increased in pancreatic tissue after an LPS injection. Apoptosis in p ancreatic acinar cells and fragmentation of DNA typical of apoptosis i n pancreatic tissue was seen 24 hours after an LPS injection. Pancreat ic acinar atrophy was seen 72 hours after the LPS injection. Conclusio ns-These data show that LPS causes release of pancreatic PLA(2) into b lood plasma, activation of PLA(2) in pancreatic tissue, and apoptosis of acinar cells.