Involvment of Endogenous Prostaglandin in Emodin-Evoked Rat Colonic Anion Secretion

抄録

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 EC₅₀ was 76.0 μmol/l. Pretreatment with epithelial Na⁺ channel blocker, amiloride (10 μmol/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 μmol/l) decreased emodin-induced I_SC from 118.1±6.7 μA/cm² to 16.7±2.0 μA/cm², which was reduced by 85.9%. Basolateral pretreatment with neuronal Na⁺ channel blocker tetrodotoxin (TTX) (1 μmol/l) did not affect emodin-induced I_SC increase, but pretreatment with indomethacin (10 μmol/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.