Objective To observe the effect of electroacupuncture(EA) at “Zusanli”(ST36) on the phosphorylated tau levels in pancreas and hippocampus of type 2 diabetes mellitus(T2 DM) rats

so as to explore the underlying mechanism of EA in diabetic demention rats. Methods Forty-eight male Sprague-Dawley rats were randomly divided into control

model and EA groups

with 16 rats in each group. The T2 DM model was established by 6 weeks of high-fat

high-sugar diet as well as intrape-ritoneal injection of streptozocin(STZ) solution(35 mg/kg). After that

EA(2 Hz

0.1 mA) was applied to unilateral “Zusanli”(ST36) for 30 min

once a day

6 times a week for 4 weeks. The survival rate was recorded every week

and the fasting blood glucose(FBG) was detected on the 1

(st)

6(st)

6

(th)

and 11(th) and 11

(th)

week. The level of serum insulin(INS) was measured by using ELISA. The morphological structure of pancreas islet was observed by H.E. staining. The expressions of phosphorylated tau at the sites of Ser 396(pS396) and Thr 231(pT231)

total tau(Tau5)

phosphorylated glycogen synthase kinase-3β(pGSK-3β) and total glycogen synthase kinase-3β(GSK-3β) in pancreas and hippocampus were detected by Western blot. The expression and distribution of pS396 and pT231 in pancreas and hippocampus were assayed with immunohistochemistry.Results Compared with the control group

the survival rate presented a significant decline

the contents of FBG and INS were obviously higher(P

<

0.01)

and the structure of the pancreas islet appeared shrunken

obscure and disordered in the model group. Furthermore

the levels of pS396

pT231 in pancreas and hippocampus were obviously higher in the model group(P

<

0.01)

while the level of pGSK-3β in pancreas and hippocampus was significantly lower in the model group(P

<

0.01). In comparison with the model group

the survival rate of EA group was higher. Following 4 weeks' interventions

the enhanced levels of tau phosphorylation and GSK-3β activity in pancreas and hippocampus were partly reversed in the EA group compared to the model group(P

<

0.05

P

<

0.01). Conclusion EA at ST36 can reduce the level of tau phosphorylation via regulating the activity of GSK-3β in the pancreas and hippocampus of T2 DM rats

which may be related with the effect of EA on the brain function in T2 DM rats.