Lipopolysaccharide induced apoptosis of rat pancreatic acinar cells

被引：51

作者：

Laine, VJO ^{[1
]}

Nyman, KM ^{[1
]}

Peuravuori, HJ ^{[1
]}

Henriksen, K ^{[1
]}

Parvinen, M ^{[1
]}

Nevalainen, TJ ^{[1
]}

机构：

[1] UNIV TURKU,DEPT ANAT,TURKU 20520,FINLAND

来源：

GUT | 1996年 / 38卷 / 05期

关键词：

apoptosis; acinar cell; lipopolysaccharide; pancreas; phospholipase A(2);

D O I：

10.1136/gut.38.5.747

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Background-Bacterial lipopolysaccharide (LPS) has been proposed to participate in the pathogenesis of pancreatic inflammatory disease. Aims-This study investigated the role of endotoxaemia in the pathogenesis of pancreatic acinar cell injury. Methods-Sixty eight male Spraque-Dawley rats were used in the study. Escherichia coli LPS (5 mg/kg) was injected into the peritoneal cavity of the rats. The concentration of pancreatic phospholipase A(2) (PLA(2)) in plasma was measured and pancreatic tissue examined by histology, in situ detection of free DNA 3'-ends, and electrophoretic DNA analysis. Results-The concentration of pancreatic PLA(2) increased in plasma and the catalytic activity of PLA(2) increased in pancreatic tissue after an LPS injection. Apoptosis in pancreatic acinar cells and fragmentation of DNA typical of apoptosis in pancreatic tissue was seen 24 hours after an LPS injection. Pancreatic acinar atrophy was seen 72 hours after the LPS injection. Conclusions-These data show that LPS causes release of pancreatic PLA(2) into blood plasma, activation of PLA(2) in pancreatic tissue, and apoptosis of acinar cells.

引用

页码：747 / 752

页数：6

共 43 条

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