Involvement of endogenous prostaglandin in emodin-evoked rat colonic anion secretion.

It has been reported that emodin is able to promote gastrointestinal motility and stimulate large intestinal water secretion; however, the mechanism is still not clear. The aim of the present study is to examine the effects of emodin on the rat colonic transepithelial ion transport and the underlying mechanism. The study was carried out by means of the short circuit current (I(SC)) recording. Basolateral application of emodin induced a concentration-dependent I(SC) increase, and the EC(50) was 76.0 micromol/l. Pretreatment with epithelial Na(+) channel blocker, amiloride (10 micromol/l), did not affect the I(SC) responses elicited by emodin, but removal of extracellular Cl(-) or apical pretreatment with Cl(-) channel blocker, glibenclamide (1 mmol/l) inhibited emodin-elicited I(SC) responses by 76.3% and 83.8% respectively. Inhibiting basolateral Na(+)-K(+)-2Cl(-) cotransporter (NKCC) with bumetanide (100 micromol/l) decreased emodin-induced I(SC) from 118.1+/-6.7 microA/cm(2) to 16.7+/-2.0 microA/cm(2), which was reduced by 85.9%. Basolateral pretreatment with neuronal Na(+) channel blocker tetrodotoxin (TTX) (1 micromol/l) did not affect emodin-induced I(SC) increase, but pretreatment with indomethacin (10 micromol/l) alone or with both TTX and indomethacin significantly decreased emodin-induced I(SC) increase by 88.4 and 81.2%, respectively. The present study demonstrated that emodin was able to stimulate rat colonic epithelial Cl(-) secretion, which was predominantly mediated by endogenous prostaglandin release.