中文摘要：

目的探讨大黄素对大鼠结肠跨膜转运及其可能机制。方法采用短路电流（short circuit current，ISC）技术，体外测量动物跨膜电流及电阻变化的方法。结果在基底膜侧使用大黄素（1．0、10、100、500和1000μmol·L^-1），其短路电流变化呈现浓度依赖增加，△ISC的增加分别是（17．8±3．7）μA·cm^-2（n=4）、（52．5±3．5）μA·cm^-2（n=7）、（124．9±12．0）μA·cm^-2（n=10）、（169．0±21．4）μA·cm^-2（n=12）和（251．8±36．2）μA·cm^-2（n=9），EC50为76．0μmol·L^-1；而跨膜电阻在大黄素浓度为1、10和100μmol·L^-1以下时无明显变化，当大黄素浓度达到500μmol·L^-1和1．0mmol·L^-1时，膜电阻明显降低，分别从（41．2±4．4）Ω·cm^2和（44．5±5．4）Ω·cm^2降至（26．3±2．5）Ω·cm^2和（23．4±2．3）Ω·cm^2。在顶膜侧使用上皮Na^＋通道阻断剂阿米洛利预处理后，对100．0μmol·L^-1大黄素引起的ISC变化无明显影响。在去除Cl^-的Krebs溶液中，大黄素100．0μmol·L^-1引起的ISC变化降低约76．3％（P〈0．01）。结论大黄素能够促进结肠的阴离子Cl^-分泌，而对阳离子Na^＋的吸收影响较小。

英文摘要：

Aim To examine the effects of emodin on the rat colonic transepithelial ion transportation and the underlying mechanism. Methods The study was carried out by mean of the short circuit current （ISC） recording,measuring the membrane current and transepithelial resistance in vitro. Results The basolateral emodin induced Isc response was concentration-dependently increased. When the dose of emodin was 1.0,10, 100,500 and 1000 μmol · L^-1 ,the lsc increase evoked byemodin was （17.8 ＋3.7） μA · cm^-2（n =4）, （52.5±3.5） μA · cm^-2（n =7）,（124.9 ±12.0） μA · cm^-2（n=10 ）,（169.0±21.4）μA · cm^-2（n =12） and （251.8 ±36.2） μA · cm^-2（n=9）,respectively,with an apparent EC50 of about 76.0 μmol · L^-1. The transepithelial resistance was not significantly affected when the coneentration of emodin was lower （ 1,10,100 μmol · L^-1 ） , but when the dose of emodin was heightened to 500 μmol · L^-1 and 1.0 mmol · L^-1,the resistance was significantly reduced to （26.3±2.5） Ω·cm^2 from （41.2±4.4）Ω·cm^2 （ n = 6, P 〈0. 05 ）, and to （23.4 ±2.3 ）Ω·cm^2 from （44.5±5.4）Ω·cm^2 （n=6,P〈0.01） respective-ly. Pretreatment with epithelial Na ^＋ channel blocker, amiloride （10 μmol · L^-1, apical）, did not affect the Isc responses elicited by emodin, but removal of extracellular Cl^- , inhibited emodin-elicited ISC responses by 76. 3 % （P 〈 0. 01 ）. Conclusions The results demonstrated that emodin added basolateral but not apical side was able to stimulate rat colonic epithelial Cl^- secretion,which did not affect the Na^＋ absorption elicited by emodin.