Objective To observe the effect of early electroacupuncture(EA) intervention on ionized calcium binding adapter molecule 1(Iba-1)

tyrosine hydroxylase(TH) and tumor necrosis factor-α(TNF-α) in Parkinson's disease(PD) mice

so as to explore its neuroinflammation mechanism in treating PD. Methods A total of 24 male C57 BL/6 J mice(9 weeks old) were randomly divided into control

model and EA groups

with 8 mice in each group. The PD model was established by long-term low dose subcutaneous injection of rotenone. Started at the same time with modeling

EA(2 Hz/100 Hz

1 mA) was applied to “Shenting”(GV24)

bilateral “Tianshu”(LI11)

“Quchi”(ST25)

and “Shangjuxu”(ST37) for 15 min

once a day for 8 weeks. The motor function was assessed by rotorod test and step length test. The expression levels of Iba-1 and TH proteins in substantia nigra pars compacta(SNpc) was detected by Western blot and immunohistochemistry. The expression level of TNF-α protein in colon tissue was examined by Western blot and immunofluorescence staining. Results Compared with the control group

the fall latency shortened at 4

6

and 8 weeks after modeling(P<0.01) and the step length of hind limbs shortened at 5 and 7 weeks after modeling(P<0.01)

the expression levels of Iba-1 in SNpc and TNF-α in colon tissue were increased(P<0.01)

and the expression level of TH in SNpc was decreased(P<0.01) in the model group. Compared with the model group

the fall latency prolonged at 6 and 8 weeks after modeling(P<0.01) and the step length of hind limbs prolonged at 5 and 7 weeks after modeling(P<0.01)

the expression levels of Iba-1 in SNpc and TNF-α in colon tissue were decreased(P<0.01

P<0.05)

and the expression level of TH in SNpc was increased(P<0.05

P<0.01) in the EA group. Conclusion Early EA intervention can delay the occurring time of motor disfunction

alleviated the loss of substantia nigra dopaminergic neurons

and exerted a good neuroprotective effect on the degenerative changes in rotenone-induced PD mice

which may be related to its effects in alleviating the intestinal inflammation

inhibiting the activation of microglia

thereby reducing the neuroinflammation.