Planta Med 1994; 60(4): 308-312
DOI: 10.1055/s-2006-959490

© Georg Thieme Verlag Stuttgart · New York

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

L. L. Yu1 , J. F. Liao1 , C. F. Chen1
  • 1Department & Institute of Pharmacology, National Yang-Ming Medical College, Taipei, Taiwan
  • 2National Research Institute of Chinese Medicine, Shin-Dian, Taiwan
Further Information

Publication History



Publication Date:
04 January 2007 (online)


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 µg/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 α2-, α1, or β-adrenoceptor antagonist, i.e. yohimbine (l0 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 µM 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 snowed that EF (1-50 mg/ml) significantly competed with [3 H]-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 α2, α1-, and β-adrenoceptors in the small intestine.