Objective To observe the effect of moxibustion on visceral pain

diarrhea

colonic 5-hydroxytryptamine(5-HT) content

and expression of tryptophan hydroxylase 1(TPH1)

serotonin reup take transporter(SERT) and 5-hydroxytryptamine receptor 3(5-HT3 R) in colon tissue of rats with diarrhea irritable bowel syndrome(IBS-D)

so as to reveal its underlying mechanisms in treating IBS-D. Methods Thirty male SD rats were randomly divided into blank control

model and moxibustion groups(n=10 rats in each group). The IBS-D model was established by chronic restraint combined with gavage of Senna leaf solution. Moxibustion was applied to bilateral "Tianshu"(ST25) and "Shangjuxu"(ST37) for 30 min

once a day for 7 days. After the treatment

the loose stool rate(number of loose stool/total number of feces granules X100%) and the minimum volume threshold of abdominal reflex(abdominal pain threshold) induced by rectal dilatation were observed. The content of colonic 5-HT was detected by using ELISA

and the expression of TPH1

SERT and 5-HT3 R mRNAs and proteins were detected by using quantitative real time-PCR and Western blot

respectively. Results Compared with the blank control group

the minimum volume threshold of abdominal retraction reflex and the relative expression of SERT protein and mRNA were significantly decreased(P<0.01)

and the loose stool rate

colonic 5-HT content

and relative expression of TPH1 and 5-HT3 R proteins and mRNAs were notably increased in the model group(P<0.01). After moxibustion

both the decrease of minimum volume threshold and SERT protein and mRNA expressions and the increase of loose stool rate

colonic 5-HT content and TPH1 and 5-HT3 R protein and mRNA expressions were reversed(P<0.01). Conclusion Moxibustion of ST25 and ST37 can relieve abdominal hypersensitivity and diarrhea in IBS-D model rats

which is related to its effects in down-regulating colonic 5-HT content and expression of TPH1 and 5-HT3 R proteins and mRNAs and in up-regulating expression of SERT protein and mRNA(regulating 5-HT/5-HT3 R signaling).