《中国康复理论与实践》

《中国康复理论与实践》 ›› 2003, Vol. 9 ›› Issue (09): 545-547.

• 基础研究 • 上一篇    下一篇

Ach和ATP在小鼠胰岛β细胞诱导细胞内钙变化的比较

赵玉峰; 朱运龙; 周京军; 胡玉珍   

  1. 第四军医大学生理学教研室 陕西省西安市 710032
  • 收稿日期:2003-07-03 出版日期:2003-09-25 发布日期:2003-09-25

Differential effects of Ach and ATP on [Ca2+]c changes in mouse pancreatic β-cells

ZHAO Yu-feng, ZHU Yun-long, ZHOU Jing-jun, et al   

  1. Department of Phyhsiology, Fourth Military Medical Research, Xi’an 710032, Shanxi,China
  • Received:2003-07-03 Published:2003-09-25 Online:2003-09-25

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摘要： 目的探讨Ach和ATP在小鼠胰岛β细胞诱导细胞内钙([Ca2+]c)变化的不同。方法原代培养的小鼠胰岛β细胞,分为Ach和ATP诱导组。每组又分为正常对照组、EGTA处理组和ThaPsigargin处理组。正常对照组细胞不经处理即开始[Ca2+]c测定;EGTA处理组细胞加入EGTA的无钙溶液,螯合细胞外Ca2+后进行[Ca2+]c测定;ThaPsigargin处理组细胞记录前用ThaP sigargin(1mmol/L)预处理20分钟,耗竭细胞内钙库的Ca2+后进行[Ca2+]c测定。采用Fura-2钙离子指示剂反映[Ca2+]c,观察Ach与ATP诱导[Ca2+]c变化的规律。结果Ach可诱导[Ca2+]c的短暂峰性升高和持续性升高。ATP只诱导[Ca2+]c的短暂峰性升高,无持续性升高。EGTA螯合细胞外Ca2+后,Ach和ATP诱导的[Ca2+]c峰性升高依然存在,而Ach诱导的持续性升高被消除。ThaPsigargin预处理耗竭细胞内钙库的Ca2+后 ,Ach和ATP诱导的[Ca2+]c峰性升高消除,同时Ach诱导的持续性升高也被消除。结论Ach在小鼠胰岛 β细胞诱导细胞内Ca2+释放和Ca2+释放激活的Ca2+内流;ATP可诱导细胞内Ca2+释放,但阻断Ca2+释放激活的Ca2+内流。

关键词: 小鼠, 乙酰胆碱(Ach), 三磷酸腺苷(ATP), 胰岛β细胞, 细胞内钙

Abstract: ObjectiveTo identify the differences between acetylcholine(Ach)-induced increase and adenosine triphosphate(ATP)-induced increase in cytosolic free Ca2+ concentration ([Ca2+]c) in mouse pancreatic β-cells. MethodsMouse pancreatic β-cells were primarily cultured and divided into two groups,one group was stimulated by Ach and another by ATP.[Ca2+]c was recorded with Fura-2 in normal condition, chelation of extracellular Ca2+ by EGTA and depletion of intracellular Ca2+ stores by Thapsigargin.ResultsAch induced a transient peak increase and sustained increase in [Ca2+]c. ATP induced a transient peak increase and no sustained increase. Chelation of extracellular Ca2+ by EGTA eliminated the sustained increase induced by Ach, and did not eliminate the transient peak increase induced by Ach and ATP. Depletion of intracellular Ca2+ stores by Thapsigargin eliminated the transient peak increase induced by Ach and ATP and the sustained increase induced by Ach. ConclusionsAch induces intracellular Ca2+ release and the following Ca2+ release-activated Ca2+ influx, and ATP induces intracellular Ca2+ release, but blocks the following Ca2+ release-activated Ca2+ influx.

Key words: mouse, acetylcholine, adenosine triphosphate, pancreatic β-cells, intracellular Ca2+