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黄刚,汤为学,陶小红.生长抑素对大鼠胰腺腺泡细胞内骨架蛋白F-actin分布和细胞外分泌功能的影响[J].陆军军医大学学报(原第三军医大学学报),2010,32(07):672-676.
Huang Gang,Tang Weixue,Tao Xiaohong.Effect of somatostatin on F-actin distribution and exocrine function in rat pancreatic acinar cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(07):672-676.
黄刚,汤为学,陶小红.生长抑素对大鼠胰腺腺泡细胞内骨架蛋白F-actin分布和细胞外分泌功能的影响[J].陆军军医大学学报(原第三军医大学学报),2010,32(07):672-676. DOI:
Huang Gang,Tang Weixue,Tao Xiaohong.Effect of somatostatin on F-actin distribution and exocrine function in rat pancreatic acinar cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(07):672-676. DOI:
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Factin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
-8
mol/L)、SS组(10
-7
mol/L)、SS+CCK-8组。SS与不同浓度的CCK-8共同孵育胰腺腺泡细胞30 min,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(P0.05);SS与低浓度的CCK-8(10
-11
~10
-10
mol/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(P0.05),SS与高浓度CCK-8(10
-9
~10
-8
mol/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(P0.05)。 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 investigated the effect of somatostatin (SS) on cholecystokinin-induced alterations of exocrine function and the redistribution of the F-actin in the pancreatic acinar cells. Methods In vitro
isolated rat pancreatic acini were divided into 12 groups: normal control group
different concentrations of cholecystokinin-octapep
tide groups (CCK-8) of 10
-12
10
-11
10
-10
10
-9
or 10
-8
mol/L
SS group (10
-7
mol/L)
SS and different dose CCK-8 groups. The acinar cells were stimulated with different concentrations of CCK-8 for 30 min in the presence or absence of 10
-7
mol/L SS. Amylase and trypsin activity were measured using corresponding assay kits
and F-actin distribution in pancreatic acinar cells were detected by laser confocal microscopy. Results SS stabilized the structure of cytoskeleton in acinar cells
and remarkably increased the ratio of subapical/basolateral F-actin (P0.05); Exposure to low concentrations of CCK-8 (10
-11
to 10
-10
mol/L) in the presence of SS
the CCK-induced amylase release were significantly inhibited (P0.05). However
at higher concentrations of CCK-8 (10
-9
to 10
-8
mol/L)
the CCK-induced inhibition of amylase release was not observed as SS present
and SS significantly inhibited CCK-stimulated trypsin activity in acinar cells (P0.05). Conclusion SS stabilizes the cytoskeleton morphology in the acinar cells
and prevents the trypsinogen activation
which might be one of the protective mechanisms of SS on CCK-induced acute injury in acinar cells.
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