氟西汀在麦迪逊-达比犬肾细胞中诱导的Ca2+信号。

Fluoxetine-induced Ca2+ signals in Madin-Darby canine kidney cells.

作者信息

Tang K Y, Cheng J S, Lee K C, Chou K J, Huang J K, Chen W C, Jan C R

机构信息

Department of Psychiatry, Kaohsiung Veterans General Hospital, Taiwan.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 2001 Jan;363(1):16-20. doi: 10.1007/s002100000337.

DOI:10.1007/s002100000337

PMID:11191831

Abstract

The effect of fluoxetine on Ca2+ signaling in Madin-Darby canine kidney (MDCK) cells was investigated by using fura-2 as a Ca2+ probe. Fluoxetine increased [Ca2+]i concentration-dependently between 5 microM and 200 microM with an EC50 value of 40 microM. The response was reduced by external Ca2+ removal by 30%40%. In Ca2+-free medium pretreatment with 1 microM thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+ pump, abolished 100 microM fluoxetine-induced Ca2+ release. Addition of 3 mM Ca2+ to Ca2+-free medium increased [Ca2+]i when cells were pretreated with 100 microM fluoxetine. Suppression of 1,4,5-trisphosphate (IP3) formation by 2 microM U73122 (a phospholipase C inhibitor) did not affect 100 microM fluoxetine-induced Ca2+ release. Fluoxetine (5-100 microM) also increased [Ca2+]i in neutrophils, prostate cancer cells and bladder cancer cells from human and rat glioma cells.

摘要

以fura-2作为钙离子探针，研究了氟西汀对麦迪逊-达比犬肾（MDCK）细胞中钙离子信号的影响。氟西汀在5微摩尔至200微摩尔之间以浓度依赖性方式增加细胞内钙离子浓度（[Ca2+]i），半数有效浓度（EC50）值为40微摩尔。去除细胞外钙离子后，该反应降低了30%至40%。在内质网钙离子泵抑制剂1微摩尔毒胡萝卜素预处理的无钙培养基中，100微摩尔氟西汀诱导的钙离子释放被完全消除。当细胞用100微摩尔氟西汀预处理后，向无钙培养基中添加3毫摩尔钙离子会增加细胞内钙离子浓度。2微摩尔U73122（一种磷脂酶C抑制剂）抑制1,4,5-三磷酸肌醇（IP3）的形成，并不影响100微摩尔氟西汀诱导的钙离子释放。氟西汀（5至100微摩尔）也会增加人源和大鼠源胶质瘤细胞的中性粒细胞、前列腺癌细胞和膀胱癌细胞中的细胞内钙离子浓度。