Effect of the Crude Extract of Evodiae Fructus on the Intestinal Transit in Mice

Abstract

One of the uses of Evodiae Fructus (EF, the dried, unripe fruit of Evodia rutaecarpa) in Chinese medicine is recommended in diarrhea, but its underlying mechanism has not yet been studied. The present study examined the effect of an aqueous extract of EF on the intestinal transit in mice by the charcoal meal method. Intraperitoneal administration (i.p.) of EF (1.9-30 g/kg) significantly inhibited the intestinal transit in a dose- and time-dependent manner. This inhibitory effect of EF was not attenuated by the i.p. pretreatment with an alpha 2-, alpha 1-, or beta-adrenoceptor antagonist, i.e. yohimbine (10 mg/kg), prazosin (2 mg/kg), or propranolol (6 mg/kg), respectively. In the isolated mouse duodenum, jejunum, and ileum preparations, EF (10-50 mg/ml) concentration-dependently abolished 10 microM carbachol-induced contraction with an IC50 of 9.9, 11.7, and 16.3 mg/ml, respectively. This inhibitory effect was not competitive. Receptor binding assay showed that EF (1-50 mg/ml) significantly competed with [3H]-N-methylscopolamine for specific binding to muscarinic receptors on the duodenum, jejunum, and ileum membrane preparations with a Ki value of 7.1, 8.4, and 14.4 mg/ml, respectively. Therefore, the above results suggested that the inhibitory effect of EF on intestinal transit was probably via an action directly on the muscarinic receptors but not on the alpha 2, alpha 1-, and beta-adrenoceptors in the small intestine.