【摘要】 目的　谷胱甘肽 (GSH)耗竭在各型急性胰腺炎中均有报道 ,本研究探讨GSH耗竭对胰腺外分泌的影响以及其可能的机制。方法　利尿酸和二酰胺用于减低胰腺腺细胞内GSH ,并检测GSH对蛙皮素刺激的淀粉酶释放、胆囊收缩素受体亲和力以及细胞内Ca2 + 浓度的影响。结果　 2种巯基氧化剂均可剂量依赖性减少胰腺腺细胞内GSH水平及蛙皮素 (1× 10 -10 mol/L)刺激的淀粉酶释放。二酰胺还减少蛋白巯基水平。利尿酸和二酰胺均可抑制蛙皮素 (1× 10 -9mol/L)诱导的胰腺腺细胞Ca2 + 运动。而两者对胆囊收缩素受体亲和力均无影响。结论　本研究提示GSH在胰腺腺细胞分泌过程中具有重要作用 ,并与急性胰腺炎过程中分泌阻滞的发生有关。蛙皮素诱导的Ca2 + 运动的抑制可能参与GSH耗竭对胰腺外分泌的抑制作用更多还原

【Abstract】 Objective Glutathione depletion has been described in all form of acute pancreatitis This study evaluated the effect of glutathione depletion on pancreatic exocrine secretory function and explored the potential mechanisms Methods Thiol oxidants ethacrynic acid and diamide were employed to deplete pancreatic acinar glutathione The effect of glutathione depletion on caerulein stimulated amylase release, cholecystokinin (CCK) receptor binding characteristics, and cytosolic free calcium was investigated Results Both the thiol oxidants decreased the level of pancreatic acinar glutathione and caerulein (1×10 -10 mol/L) stimulated amylase release in a dose dependent manner without a marked increase in cell damage Diamide also diminished the level of protein thiols Ethacrynic acid and diamide both inhibited the caerulein (1×10 -9 mol/L) induced Ca 2+ mobilization in pancreatic acinar cells Neither ethacrynic acid nor diamide altered the CCK receptor binding characteristics Conclusions The present findings strongly suggest that glutathione plays a potential role in the secretory process in pancreatic acinar cells and in the secretory blockade observed in acute pancreatitis A decrease of caerulein induced Ca 2+ mobilization might participate in the effect of glutathione depletion on pancreatic exocrine secretory function更多还原