中文摘要：

目的：研究脱氧胆酸钠（sodium deoxycholate，SDOC）刺激时大鼠胰腺腺泡细胞功能状态的变化并探讨其可能的信号转导途径。方法：胶原酶法分离大鼠胰腺腺泡细胞，经不同浓度的SDOC或正常培养液处理，在不同的时点（30min、1h、4h、10h）采用MTT法检测不同时点胰腺腺泡细胞的活性；采集上清液检测其中丙二醛含量以及超氧化物歧化酶的活性；另外细胞经Fluo-3／AM负载后，在无钙或含生理钙离子浓度的培养液中以灌流的方式加入不同浓度SDOC，采用激光共聚焦显微镜观察单个胰腺腺泡细胞[Ca^2＋]i。结果：SDOC导致胰腺腺泡细胞的存活率降低、且呈时间及浓度依赖性（P〈0．05），1mmol／L依他酸（egtazic acid，EGTA）使SDOC诱发的腺泡细胞损伤程度明显减轻（P〈0．05）；在无钙且含1mmol／LEGTA的培养液中SDOC未见引起胞浆[Ca^2＋]i的变化，再次恢复培养液中的钙离子浓度至生理水平，SDOC引发胞浆[Ca^2＋]i迅速升高；腺泡细胞内[Ca^2＋]i的变化明显先于细胞培养上清中的生化改变和腺泡细胞的损伤；与对照组相比，SDOC组胰腺腺泡细胞上清液中丙二醛含量增加（P〈0．05），超氧化物歧化酶活性明显降低（P〈0．05）。结论：SDOC可致胰腺腺泡损伤，且对刺激时间、刺激剂浓度及胞浆钙离子具有依赖性；SDOC通过促进胞外Ca^2＋的内流导致胰腺腺泡胞浆内钙超载。钙超载作为早期的病理事件通过过氧化反应参与腺泡细胞损伤的发生，钙稳态失衡是SDOC致胰腺细胞损伤的主要因素之一。

英文摘要：

AIM ： To investigate the alteration of functional state of pancreatic aeinar cells stimulated by sodium deoxycholate （SDOC）, and to explore the possible signal pathway involved in the effects of SDOC. METHODS： Rat pancreatic acinar cells were isolated by collagenase digestion and were treated with varying concentration of SDOC or culture media respectively. At different time points （30 min, 1 h, 4 h, 10 h） , cell viability was determined by MTT and supernatant of cells was collected to measurer the content of maloidialdehyde （MDA） and the activity of superoxide dismutase （SOD）. Some cells were loaded with Fluo -3/AM, then exposed to varying doses of SDOC. [Ca^2＋]i change of single pancreatic acinar cell in extracellular fluid with the absence or presence of Ca^2＋ was determined by laser scanning confocal microscopy. RESULTS ： SDOC initiated cell damage in a time - and concentration - dependent manner （ P 〈 0. 05 ）. Egtazic acid （EGTA） at the concentration of 1 mmol/L decreased the cell mortality （ P 〈 0. 05 ）. SDOC did not induce a rise of [ Ca^2＋ ]i in the calcium - free extracellular fluid. Addition of extracellular calcium in the presence of SDOC resulted in a rapid and remarkable rise of [ Ca^2＋ ]i. The increase in [ Ca^2＋ ]i preceded the pathological and biological alteration of pancreatic acinar cells. The supernatant content of MDA increased （ P 〈 0. 05） and the supernatant activity of SOD decreased in SDOC group（P 〈 0. 05）. CONCLUSION： SDOC initiates cell damage in a time, concentration and calcium dependent manner. SDOC only induces the influx of Ca^2＋ from extracellular fluid. Calcium overload as an early pathogenetic event takes part in the damage of pancreatic acinar cells by the response of superoxidation. Calcium homeostasis disorder may be one of the causes or at least an important mediator of SDOC - induced pancreatic acinar cell damage.