Objective: To investigate the pathogenesis of functional dyspepsia with spleen deficiency

and explore the intervening mechanism of Sijunzi Tang. Method: Fifty-two male SD rats were randomly divided into normal group

model group

Sijunzi Tang group and mosapride group. Iodoacetamide gavage method

small platform standing method and hunger disorder method were used to establish the functional dyspepsia rat model with spleen-deficiency. After modeling

Sijunzi Tang (6.3 g·kg-1) and mosapride (0.45 mg·kg-1) were given to each intervention group by gavage

once a day

for continuously 14 days. Gastric emptying rate

C-type natriuretic peptide(CNP) and cGMP content were detected by enzyme-linked immunosorbent assay(ELISA)

and natriuretic peptide receptor type B(NPR-B) was determined by Western blot. Result: Compared with normal group

weight and gastric emptying rate were lower (P<0.05

P<0.01)

CNP content in serum

NPR-B protein expression in gastric antrum smooth muscle

and cGMP content of gastric smooth muscle were higher in model group (P<0.05

P<0.01). Compared with model group

gastric emptying rate was higher (P<0.05)

CNP content in serum

NPR-B protein expression in gastric antrum smooth muscle

cGMP content of gastric smooth muscle were lower in Sijunzi Tang group and mosapride group (P<0.05

P<0.01). Conclusion: Functional dyspepsia rats with spleen deficiency show CNP-NPRB-cGMP pathway disorder. Sijunzi Tang may improve gastrointestinal motility by regulating CNP-NPRB-cGMP pathway.