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目的研究生长抑素(somatostatin,SS)对八肽胆囊收缩素(cholecystokinin-octapeptide,CCK-8)刺激的大鼠胰腺腺泡细胞内骨架蛋白F-actin分布变化和细胞外分泌功能的影响。方法分离的19只SD大鼠胰腺腺泡细胞,设空白对照组、不同浓度CCK-8组(10-12、10-11、10-10、10-9、10-8mol/L)、SS组(10-7mol/L)、SS+CCK-8组。SS与不同浓度的CCK-8共同孵育胰腺腺泡细胞30min,用淀粉酶、胰蛋白酶试剂盒检测胰腺腺泡细胞淀粉酶分泌率、胰蛋白酶活性,用激光共聚焦显微镜观察细胞内F-actin分布的变化。结果SS稳定了细胞内骨架蛋白结构,明显提高F-actin近细胞顶部/侧基底部的比值(P<0.05);SS与低浓度的CCK-8(10-11~10-10mol/L)共同孵育胰腺腺泡细胞时,CCK-8诱导的细胞淀粉酶分泌明显被抑制(P<0.05),SS与高浓度CCK-8(10-9~10-8mol/L)共同孵育胰腺腺泡细胞时,缓解了高浓度CCK-8诱导的对细胞淀粉酶分泌的抑制效应;SS降低了CCK-8诱导的胰腺腺泡细胞内胰蛋白酶的活性(P<0.05)。结论SS稳定了骨架蛋白的结构,阻止了腺泡细胞内胰蛋白酶原的激活,这可能是SS对CCK-8诱导的急性胰腺炎腺泡细胞损伤的保护机制之一。
Objective To investigate the effect of somatostatin (SS) on the distribution and extracellular secretion of F-actin in rat pancreatic acinar cells stimulated by octapeptide cholecystokinin-octapeptide (CCK-8). Methods Nineteen SD rat pancreatic acinar cells isolated from rats were divided into blank control group, CCK-8 group (10-12,10-11,10-10,10-9,10-8 mol / L), SS group (10-7mol / L), SS + CCK-8 group. SS and different concentrations of CCK-8 were incubated with pancreatic acinar cells 30min, with amylase, trypsin kit detection of pancreatic acinar cell amylase secretion rate, trypsin activity, confocal laser scanning microscope intracellular F-actin distribution The change. Results SS could stabilize the structure of intracellular cytoskeleton and significantly increase the ratios of apical / lateral base of F-actin (P <0.05). SS was associated with low concentration of CCK-8 (10-11-10-10 mol / L) When incubated with pancreatic acinar cells, the secretion of amylase induced by CCK-8 was significantly inhibited (P <0.05). When SS was incubated with high concentration of CCK-8 (10-9-10-8 mol / L) , Alleviated the inhibitory effect of high concentration of CCK-8 on the secretion of amylase. SS reduced the activity of trypsin induced by CCK-8 in pancreatic acinar cells (P <0.05). Conclusion SS stabilizes the structure of skeletal proteins and prevents the activation of trypsinogen in acinar cells. This may be one of the protective mechanisms of SS against CCK-8-induced acute pancreatitis in acinar cells.