Objective To observe the effect of electroacupuncture(EA) on behavior

tyrosine hydroxylase(TH)

mitochondrial complexes Ⅰ—Ⅳ

mitochondrial membrane potential and mitochondrial ultrastructure of Parkinson's disease(PD) mice

so as to explore its mechanism underlying improvement of PD. Methods C57 BL/6 mice were randomly divided into normal

model

medication(Madopar) and EA groups(n=11 in each group). PD model was duplicated by intraperitoneal injection of 1-methyl-4-phenyl-1

2

3

6-tetrahydropyridine(MPTP

30 mg·kg

(-1)

·d(-1)·d

(-1)

) for consecutively 5 d. EA was performed on the chorea tremor areas on both sides of the head of mice for 15 min

once a day for 14 d. The behavioral changes of mice were observed. The expression of TH in substantia nigra compacta of midbrain was detected by immunohistochemistry. The activities of mitochondrial complexes Ⅰ—Ⅳ were measured. The changes of mitochondrial membrane potential were detected by JC-1 staining method. The ultrastructural changes of striatum mitochondria were observed by transmission electron microscope. Results After modeling

the mice showed obvious behavioral abnormalities such as tremor

vertical hair and tail warping

and the pole test time in the model group was significantly longer than that in the normal group(P

<

0.01). After 7 and 14 days of the treatment

the pole test time in the EA and medication groups was shorter than that in the model group(P

<

0.05

P

<

0.01). Compared with the normal group

the number of TH positive cells of the substantia nigra

the mitochondrial membrane potential and the activity of mitochondrial complex I were decreased significantly in the model group(P

<

0.01)

and EA and medication intervention reversed these changes(P

<

0.01). The mitochondrial structure of mice in the model group was obviously damaged

and the damage of mitochondrial structure was alleviated and the number of damaged mitochondria was decreased in the EA and medication groups. Conclusion EA can protect and promote the recovery of mitochondrial structure and function in MPTP-induced PD mice

which may play a neuroprotective effect on PD mice by improving mitochondrial dysfunction

balancing cell homeostasis and reducing dopaminergic neuron damage.