Objective To explore the mechanism of electroacupuncture(EA) at “Zusanli”(ST36) on improving glucose metabolism disorder in chronic restraint induced depressed rats. Methods A total of 30 male SD rats were randomly divided into control

model and EA groups

with 10 rats in each group. The depression model was established by chronic restraint 2.5 h each day for 4 weeks. For rats in the EA group

EA stimulation(1 mA

2 Hz

30 min) was applied to bilateral ST36 during the modeling period

once a day for 4 weeks. The body weight of the rats was recorded before and after modeling. The behavior of rats was observed by sugar-water preference and forced swimming after modeling. The contents of glucose and glycosylated albumin in serum were determined by biochemical method. The histopathological morphology and liver glycogen content were observed by HE and PAS staining. The expression levels of phosphatidylinositol 3-kinase(PI3K)

phosphorylated(p)-PI3K(p-PI3K)

protein kinase B(Akt)

p-Akt

glycogen synthase kinase-3β(GSK3β) and p-GSK3β proteins in liver were determined by Western blot. Results Compared with the control group

the weight increment and sugar-water preference index decreased(P<0.01)

the immobile swimming time was prolonged(P<0.01)

the glucose and glycosylated albumin contents in serum increased(P<0.05)

the expression of p-Akt protein and the ratio of p-Akt/Akt in liver tissues decreased(P<0.001)

the expression of p-GSK3β protein and the ratio of p-GSK3β/GSK3β in liver tissues increased(P<0.01

P<0.001) in the model group. Compared with the model group

the weight increment and sugar-water preference index increased(P<0.05)

the immobile swimming time was shortened(P<0.05)

the glucose and glycosylated albumin contents in serum decreased(P<0.05)

the expressions of p-PI3K and p-Akt proteins and the ratio of p-PI3K/PI3K and p-Akt/Akt in liver tissues increased(P<0.05)

the expression of p-GSK3β protein and the ratio of p-GSK3β/GSK3β in liver tissues decreased(P<0.01) in the EA group. HE staining showed that the structure of the hepatic lobule was intact

no obvious inflammatory cell infiltration or fibrosis was observed in the lobule and interstitium

and no abnormalities were observed in the small bile duct

portal vein and artery in the portal area. PAS staining showed that the intensity of staining from the center of the hepatic lobule to the periphery of the hepatic lobule was gradually enhanced in the blank group

that is

the glycogen-rich granules in the hepatic cells were gradually increased; most of the hepatocytes were light colored and glycogen was lost significantly in the model group; while the intensity of hepatocyte staining increased

the staining intensity of the perilobular zone was weaker than that in the blank group

and the glycogen particles partially recovered in the EA group. Conclusion EA intervention can regulate glucose metabolism disorder in chronic restraint induced depressed rats through PI3K/Akt/GSK3β signaling pathway.