Ethacrynic acid inhibits pancreatic exocrine secretion  

依他尼酸抑制胰腺外分泌(英文)

作　　者：YU Hong-Gang, KLONOWSKI-STUMPE Hanne ( Division of Gastroenterology, Hepatology, and Infectious Diseases, Department of Medicine, Heinrich-Heine-University of Duesseldorf, Duesseldorf, Germany)Department of Medicine,St-Josef Hospital,University of Bochum,Gudrunstr 56,44791 Bochum,Germany 

机构地区：[1]Division of Gastroenterology, Hepatology, and Infectious Diseases, Department of Medicine, Heinrich-Heine-University of Duesseldorf, Duesseldorf, Germany

出　　处：《Acta Pharmacologica Sinica》2001年第11期961-965,共5页中国药理学报（英文版）

基　　金：Project supported by a grant from "Freunde und Frderer der Heinrich-Heine-Universitt"

摘　　要：AIM: The effect of ethacrynic acid on pancreatic exocrine secretion function and potential mechanisms of interference with the secretory process in pancreatic acinar cells were investigated. METHODS: After incubation with ethacrynic acid for 30 min, caerulein-stimulated amylase release and cholecystokinin (CCK) receptor binding characteristics were assessed in isolated rat pancreatic acini. The level of thiol groups (glutathione and protein thiols) and cytosolic free calcium were measured in pancreatic acinar cells. RESULTS: Ethacrynic acid decreased caerulein (0.1 nmol/L)-stimulated amylase release and the level of pancreatic acinar glutathione in a concentration-dependent fashion without a marked increase in cell damage. Ethacrynic acid also inhibited the caerulein (1 nmol/L)-induced Ca2+ mobilization in pancreatic acinar cells. But neither protein thiol nor CCK-receptor binding characteristics was altered by ethacrynic acid. CONCLUSION: Ethacrynic acid inhibit pancreatic exocrine secretion by depletion of glutathione and down-regulation of caerulein-induced Ca2+ mobilization. Glutathione might play a potential role in the secretory process in pancreatic acinar cells and in the secretory blockade observed in acute pancreatitis.瞄准：胰腺的外分泌分泌物上的 ethacrynic 酸的效果工作，有在胰腺的腺泡房间的能分泌的过程的干扰的潜在的机制被调查。方法：在有为 30 的 ethacrynic 酸的孵化以后， min，刺激 caerulein 的淀粉酶版本和缩胆囊素(CCK ) 受体绑定特征在孤立的老鼠被估计胰腺的腺泡。巯基组(谷胱甘肽和蛋白质 thiols ) 和 cytosolic 的水平免费的钙在胰腺的腺泡房间被测量。结果：Ethacrynic 酸减少了没有房间损坏的显著增加， caerulein (0.1 nmol/L ) 以一种集中依赖者方式刺激了淀粉酶版本和胰腺的腺泡谷胱甘肽的水平。Ethacrynic 酸也禁止了导致的 caerulein (1 nmol/L ) 在胰腺的腺泡房间的 Ca2+ 动员。但是既不蛋白质巯基也不 CCK 受体绑定特征被 ethacrynic 酸改变。结论：Ethacrynic 酸由谷胱甘肽的弄空和导致 caerulein 的 Ca2+ 的下面规定禁止胰腺的外分泌分泌物动员。谷胱甘肽可能在胰腺的腺泡房间并且处于在尖锐胰腺炎观察的能分泌的封锁在能分泌的过程起一个潜在的作用。

关 键 词：AMYLASES Animals Biological Transport  Active CAERULEIN Calcium Cells  Cultured Depression  Chemical DOWN-REGULATION Enzyme Inhibitors Ethacrynic Acid Glutathione Male Pancreas RATS Rats  Wistar Receptors  Cholecystokinin Research Support  Non-U.S. Gov't 

分 类 号：R96[医药卫生—药理学]