Objective To explore the interventional mechanism of electroacupuncture(EA) of “Zusanli”(ST36)based on the involvement of mast cells/transient receptor potential vanilloid type1(TRPV1) signaling pathway in relieving visceral hypersensitivity in functional dyspepsia(FD) rats. Methods Sixty SD rats(half male and half female

10 days in age) were randomly divided into normal control

model

medication(ketotifen) and EA groups

with 15 rats in each group. The FD model was established by gavage of iodoacetamide combined with tail clamping(stress stimulation). Rats of the medication group received intraperitoneal injection of ketotifen(1 mg·kg

(-1)

·d(-1)·d

(-1)

) for 14 d

and those of the EA group received EA of ST36 for 20 min

once a day for 14 d. An air-balloon was inserted into the rat's stomach for recording changes of the intragastric pressure(mL/mm Hg) via a pressure transducer. The visceral hypersensitivity was assessed using abdominal withdrawal reflex(AWR) score and the number and degranulation of mast cells of gastric mucosa were observed using toluidine blue staining. The expression levels of TRPV1 and proteinase activated receptor 2(PAR2) in the stomach were observed using immunofluorescence histochemistry and Western blot

separately

and the contents of SP and CGRP in the stomach detected using ELISA. Results When the intragastric pressure was at 50

60 and 70 mm Hg

the gastric compliance was significantly decreased(P

<

0.01)

and the levels of visceral sensitivity increased in the model group(P

<

0.01). TRPV1 immunofluorescence tensity

expression of PAR2 and TRPV1 proteins

and contents of SP and CGRP in the stomach were considerably up-regulated in the model group compared with the normal control group(P

<

0.01). In comparison with the model group

under intragastric pressure of 50

60 and 70 mm Hg

the gastric compliance was obviously increased

and the visceral hypersensitivity decreased in the EA group(P

<

0.01

P

<

0.05). TRPV1 immunofluorescence intensity

expression levels of PAR2 and TRPV1 proteins

and the contents of SP and CGRP in the stomach were considerably down-regulated in both medication and EA groups compared with the model group(P

<

0.01

P

<

0.05). The therapeutic effect of EA was significantly superior to that of medication in up-regulating the gastric compliance(at 70 mm Hg)

and down-regulating the contents of SP and CGRP(P

<

0.05). No significant differences were found between the EA and medication groups in up-regulating gastric compliance at intragastric pressure of 50 and 60 mm Hg

and in down-regulating the visceral sensitivity

TRPV1 fluorescence intensity

and expression of PAR2 and TRPV1 proteins(P

>

0.05). Toluidine blue staining showed an apparent increase of mast cell number with obvious degranulation in the gastric mucosa of rats in the model group

which was milder in the EA and medication groups. Conclusion EA of ST36 can suppress visceral hypersensitivity and increase the gastric compliance in FD rats

which may be related with its effects in inhibiting the activation of gastric mast cells

and down-regulating the expression of gastric PAR2 and TRPV1 proteins and SP and CGRP contents.