Abstract
ObjectivesUsing an atropine-diphenoxylate-induced slow transit constipation (STC) model, this study explored the effects of the total glucosides of paeony (TGP) in the treatment of STC and the possible mechanisms.Study DesignA prospective experimental animal study.MethodsThe constipation model was set up in rats with an oral gavage of atropine-diphenoxylate and then treated with the TGP. The volume and moisture content of the faeces were observed and the intestinal kinetic power was evaluated. Meanwhile, the colorimetric method and enzyme linked immunosorbent assay (ELISA) were employed to determine the changes of nitric oxide (NO), nitric oxide synthase (NOS), vasoative intestinal peptide (VIP) and the P substance (SP) in the serum, respectively. The protein expressions of c-kit and stem cell factor (SCF) were assessed by immunohistochemical analysis and western blot, respectively, and the mRNA level of c-kit was measured by a reverse transcription polymerase chain reaction (RT-PCR).ResultsThe TGP attenuated STC responses in terms of an increase in the fecal volume and moisture content, an enhancement of intestinal transit rate and the reduction of NO, NOS and VIP in the serum. In addition, the c-kit, a labeling of interstitial cells of Cajal (ICC) increased at both protein and mRNA levels. SCF, which serves as a ligand of c-kit also increased at protein level.ConclusionThe analysis of our data indicated that the TGP could obviously attenuate STC through improving the function of ICC and blocking the inhibitory neurotransmitters such as NO, NOS and VIP.
Highlights
Slow transit constipation (STC), an intractable constipation, is usually characterized by a heavily delayed colonic transit up to true colonic inertia [1]
The faeces defecated by rats in the model control group (MC) group were dry, small, hard and without burnish (Fig 1A and 1B)
The number and moisture content of faeces decreased after oral gavage of atropinediphenoxylate, whereas they increased when treated by total glucosides of paeony (TGP) (Fig 2A and 2B)
Summary
Slow transit constipation (STC), an intractable constipation, is usually characterized by a heavily delayed colonic transit up to true colonic inertia [1]. This is a very prevalent motility problem, but its aetiology has not been elucidated as yet [2]. ICC is found between the nerve endings and smooth muscle cells in the gastrointestinal (GI) tract. A decreased number of ICC might lead to absence of slow wave activity, thereby affecting the contractile response and causing delayed transit in STC patients. In this regards, amelioration of ICC function using drugs may be essential to treat STC
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
