AIM:To isolate the proteins involved in pharmacologicaction of senna extract(SE)from mouse gastrointestinaltract and to explore the molecular mechanism ofgastrointestinal motility change induced by SE,METHODS:SE was administrated to mica by differentroutes.Gastrointestinal motility of mica was observed usingcathartic,gastrointestinal propellant movement experimentsand X-ray analysis.Mouse model for gastrointestinal motilityenhancement was established through continuous gastricadministration of SE with at progressively increased close.At 3 h and week-3,4,6 and 10,morphological changes ofgastrointestinal tissues were found under light microscope.Ultrastructural changes of intestinal and colonic tissues atweek 6 were observed under transmission electronmicroscope.The colonic proteomic changes in model micawere examined by two-dimension polyacrylamide gelelectrophoresis with immobilized pH gradient isoelectricfocusing to screen the differentially expressed proteins,andtheir molecular masses and isoelectric points weredetermined.Two N-terminal sequences of the samples werealso determined by mass spectrometry.RESULTS:SE(0.3g)caused diarrhea after gastricadministration in l-6h and enhanced gastrointestinalpropellant(65.1±7.5%;45.8±14.6%,P<0.01)in mica,but intramuscular and hypodermic injection had no catharticeffect.X-ray analysis of gastrointestinal motilitydemonstrated that gastric administration of SE enhancedgastric evacuation and gastrointestinal transferring function.At 3 h and week 3 and 4 after gastric administration of SE,light microscopic examination revealed no apparent changein gastrointestinal mucosal tissues,but transmission electron microscopic examination revealed inflammatorychanges in whole layer of intestinal and colonic wall.Twenty differential proteins were detected in the colonictissues of the model mice by two-dimensionalelectrophoresis,and the N-terminal amino acid sequencesof two proteins were determined.CONCLUSION:SE causes diarrhea and enhancesgastrointestinal motility through digestive tractadministration.Long-term gastric administration of SEinduces inflammatory changes and cell damage in the wholegastrointestinal tract.The differential proteins screened fromthe colonic tissues of the model mice might mediate theenhancing effect of SE on gastrointestinal motility. AIM: To isolate the proteins involved in pharmacologicaction of senna extract (SE) from mouse gastrointestinaltract and to explore the molecular mechanism ofgastrointestinal motility change induced by SE, METHODS: SE was administrated to mica by differentroutes. Gastrointestinal motility of mica was observed using cathartic, gastrointestinal propellant movement experiments and X-ray analysis. Mouse model for gastrointestinal motility enhancement was established through continuous gastric administration of SE with progressively increased close. At 3 h and week-3, 4, 6 and 10, morphological changes of gastrointestinal tissues were found under light microscope. Ultrastructural changes of intestinal and colonic tissues atweek 6 were observed under transmission electron microscopy. The colonic proteomic changes in model micawe examined by two-dimension polyacrylamide gelelectrophoresis with immobilized pH gradient isoelectric focusing on the screen the differentially expressed proteins, and the and molecular molecular masse s and isoelectric points were determined. Two N-terminal sequences were the samples were determined by mass spectrometry. RESULTS: SE (0.3g) caused diarrhea after gastric administration in 1-6h and enhanced gastrointestinalpropellant (65.1 ± 7.5%; 45.8 ± 14.6%, P <0.01) in mica, but intramuscular and hypodermic injection had no catharticeffect. X-ray analysis of gastrointestinal motility demonstrated in gastric administration of SE enhanced gastric evacuation and gastrointestinal transferring function. At 3 h and week 3 and 4 after gastric administration of SE, light microscopic examination revealed no apparent changein gastrointestinal mucosal tissues, but transmission electron microscopic examination revealed inflammatory changes in in whole layer of intestinal and colonic wall. twenty differential proteins were detected in the colonictissues of the model mice by two-dimensionalelectrophoresis, and the N-terminal amino acid sequencesof two proteins were determined. CONCLUSION: SE causes diarrhea and enhances gastrointestinal motility through digestive tract administration. Long-term gastric administration of SEinduces inflammatory changes and cell damage in the whole gastrointestinal tract. The differential proteins screened from the colonic tissues of the model mice may mediate the enhancing effect of SE on gastrointestinal motility.