Objective To observe the effect of electroacupuncture(EA) on glucagon-like peptide-1 receptor(GLP-1 R)/phosphatidylinositol 3-kinase(PI3 K)/protein kinase B(Akt) protein pathway in the substantia nigra of mice with Parkinson's di-sease(PD)

so as to explore its underlying mechanisms in treatment of PD. Methods Forty-eight C57 BL/6 male mice were randomly divided into normal

model

EA and inhibitor groups

with 12 mice in each group. PD mouse model was established by intragastrical administration of rotenone for 4 weeks. In the EA group

EA was applied at “Fengfu”(GV16)

“Taichong”(LR3) and“Zusanli”(ST36) for 30 min

once daily

for 2 weeks. The mice of the inhibitor group received gavage of dipeptidyl peptidase-4 inhibitor ligliptin(10 mg·kg

(-1)

·d(-1)·d

(-1)

) once a day for 2 weeks. The behavioral scores of mice in each group were observed. The levels of tyrosine hydroxylase(TH) in serum and substantia nigra were detected by ELISA

and the protein relative expression levels of GLP-1 R

phosphorylation of PI3 K(p-PI3 K) and phosphorylation of Akt(p-Akt) in substantia nigra of midbrain of mice were detected by Western blot. Results Compared with the normal group

the behavioral scores were significantly increased(P

<

0.01)

TH levels in serum and substantia nigra

protein expression levels of GLP-1 R

p-PI3 K and p-Akt of the substantia nigra in the model group were significantly decreased(all P

<

0.01). After intervention and in comparison with the model group

the behavioral scores were significantly decreased(P

<

0.01)

TH levels and the protein expression levels of GLP-1 R

p-PI3 K and p-Akt in both EA and inhibitor groups were significantly increased(all P

<

0.01). There were no significant differences in the abovementioned indexes between EA group and inhibitor group(all P

>

0.05)

except for TH levels which were considerably down-regulated in the EA group relative to the inhibitor group(P

<

0.01

P

<

0.05). Conclusion EA at GV16

LR3 and ST36 may increase the level of TH in serum and substantia nigra by up-regulating the activity of GLP-1 R/PI3 K/Akt protein pathway

and improve the behavioral performance of PD induced by rotenone.