• Xiao-Li Pan, Li Zhou, Dan Wang, Yong-Li Han, Ji-Yu Wang, Pai-di Xu, and Hong-Xing Zhang.
• College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan 430061, China.
• Zhen Ci Yan Jiu. 2019 Jul 25; 44 (7): 486-91.

ObjectiveTo 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.MethodsA 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.ResultsCompared 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 down-regulating 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).ConclusionEA 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.

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