OBJECTIVE@#To investigate
autophagy-related mechanisms of
electroacupuncture (EA) action in improving
gastrointestinal motility in
mice with functional
constipation (FC).@*
METHODS@#According to a random number table, the Kunming
mice were divided into the normal control, FC and EA groups in Experiment I. The
autophagy inhibitor 3-methyladenine (3-MA) was used to observe whether it antagonized the effects of EA in Experiment II. An FC model was established by
diphenoxylate gavage. Then the
mice were treated with EA stimulation at Tianshu (ST 25) and Shangjuxu (ST 37)
acupoints. The first black stool
defecation time, the number, weight, and
water content of 8-h
feces, and intestinal transit rate were used to assess intestinal transit. Colonic
tissues underwent histopathological assessment, and the expressions of
autophagy markers
microtubule-associated protein 1 light chain 3 (LC3) and
Beclin-1 were detected by immunohistochemical
staining. The expressions of
phosphoinositide 3-
kinases (PI3K)-
protein kinase B (AKT)-
mammalian target of rapamycin (mTOR) signaling pathway members were investigated by
Western blot and quantitative
reverse transcription-
polymerase chain reaction, respectively. The relationship between enteric
glial cells (EGCs) and
autophagy was observed by confocal
immunofluorescence microscopy,
localization analysis, and
electron microscopy.@*RESULTS@#EA
treatment shortened the first black stool
defecation time, increased the number, weight, and
water content of 8-h
feces, and improved the intestinal transit rate in FC
mice (P<0.01). In terms of a putative
autophagy mechanism, EA
treatment promoted the expressions of LC3 and
Beclin-1 proteins in the colonic
tissue of FC
mice (P<0.05), with
glial fibrillary acidic protein (GFAP) and LC3 significantly colocalized. Furthermore, EA promoted colonic
autophagy in FC
mice by inhibiting PI3K/AKT/mTOR signaling (P<0.05 or P<0.01). The positive effect of EA on
intestinal motility in FC
mice was blocked by 3-MA.@*CONCLUSION@#EA
treatment can inhibit PI3K/AKT/mTOR signaling in the colonic
tissues of FC
mice, thereby promoting EGCs
autophagy to improve
intestinal motility.