Objective To explore the effect of electroacupuncture(EA)at "Zusanli"(ST36)on gastrointestinal motility and expression of autophagy marker LC3 and autophagy signaling pathway molecule AMP-activated protein kinase(AMPK)in rats with functional dyspepsia(FD)

so as to explore its mechanisms underlying improvement of FD.Methods A total of 40 male SD rats were randomly divided into blank control

model

EA

AMPK inhibitor and EA+AMPK inhibitor groups

with 8 rats in each group.The FD model was established by tail-clip(30 min/time

twice daily)+single day feeding

and gavage of normal saline(2 mL/time

twice a day)for 2 successive weeks.For rats of EA and EA+AMPK inhibitor groups

EA(4 Hz

1.0 mA)was applied to bilateral ST36 for 20 min

once daily for 7 successive days.For rats of the AMPK-inhibitor and EA+AMPK inhibitor groups

Compound C(20 mg/kg)solution was administered by intraperitoneal injection before every EA administration.The gastric residual rate and small intestinal transit rate were calculated based on the weight of stomach and length of ink propelling and total small intestine

respectively.The expression levels of c-kit

microtubule-associated protein 1 light chain 3

Beclin 1

phosphorylated(p)-AMPK and p-unc-51 like autophagy activating kinase 1(ULK1)in the gastric antrum tissue were detected by using Western blot.Results Compared with the blank control group

the gastric residual rate and the expression levels of LC3-Ⅱ/LC3Ⅰ

Beclin 1

p-AMPK and p-ULK1 proteins were significantly increased

and the small intestinal transit rate and the expression of c-kit protein obviously decreased in the model group(P<0.01).After EA intervention

modeling-induced increase of gastric residual rate and the expression of LC3-Ⅱ/LC3Ⅰ

Beclin 1

p-AMPK and p-ULK1 proteins

and decrease of small intestinal transit rate and expression of c-kit protein were reversed in the EA

AMPK inhibitor and EA+AMPK inhibitor groups(P<0.05

P<0.01).The therapeutic effect of EA and EA+AMPK was significantly superior to that of AMPK inhibitor in downregulating the expression of LC3Ⅱ/LC3Ⅰ

Beclin 1

p-AMPK and p-ULK1 proteins and in up-regulating the expression of c-kit protein(P<0.05

P<0.01).No significant differences were found among the EA

AMPK inhibitor and EA+AMPK inhibitor groups in lowering gastric residual rate and elevating the small intestinal transit rate(P>0.05).Conclusion EA at ST36 can promote gastrointestinal motility in FD rats

which is possibly mediated by inhibiting excessive autophagy of interstitial cells of Cajal via down-regulating AMPK/ULK1 signaling.