Shinozaki H, Funakoshi A, Miyasaka K, Kitani K
Social Insurance Inatsuki Hospital, Fukuoka, Japan.
Pancreas. 1995 Apr;10(3):246-50. doi: 10.1097/00006676-199504000-00005.
Ursodeoxycholate (UDCA; 300 microM) significantly stimulates amylase secretion from isolated rat pancreatic acini but not Ca2+ mobilization. Removal of extracellular Ca2+ completely abolished the UDCA-stimulated secretory response. Ca ionophore (A23187) potentiated the response. However, staurosporine, a protein kinase C inhibitor, did not affect the UDCA-stimulated amylase secretion. These results indicated that UDCA directly acted on the pancreatic acini and stimulated amylase secretion by the mechanism of stimulation of influx of extracellular Ca2+, but not through inositol [1,4,5] triphosphate and diacylglycerol formation or Ca2+ mobilization.
熊去氧胆酸(UDCA;300微摩尔)能显著刺激分离的大鼠胰腺腺泡分泌淀粉酶,但对钙离子动员无影响。去除细胞外钙离子可完全消除UDCA刺激的分泌反应。钙离子载体(A23187)可增强该反应。然而,蛋白激酶C抑制剂星形孢菌素并不影响UDCA刺激的淀粉酶分泌。这些结果表明,UDCA直接作用于胰腺腺泡,通过刺激细胞外钙离子内流的机制来刺激淀粉酶分泌,而非通过肌醇[1,4,5]三磷酸和二酰基甘油的形成或钙离子动员。