Objective To observe the effect of penetrating electro-acupuncture at scalp-acupoints on the motor function and oxidative stress action of mice with Parkinson's disease (PD).Methods Mouse model of PD was established by 5-day intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP,30 mg/kg),and then PD mice were given electro-acupuncture set at different parameters.The effect of the electroacupuncture on the behavior and expression of tyrosine hydroxylase (TH) of mice were observed to screen out the appropriate treatment parameters.Healthy C57BL/6 mice were randomly divided into blank group,model group,positive group (madopar,6.25 mg/kg) and electro-acupuncture group.The mice except for blank group were given intraperitoneal injection of MPTP to induce PD,and then the PD mice of positive group and electroacupuncture group were treated with madopar(6.25 mg/kg) and electro-acupuncture respectively from the 6th day for 7 continuous days.Behavioral test was carried out on the 5~ modeling day and on the Th electro-acupuncture treatment day to evaluate the motor function of the mice.After the mice were killed and their brains were isolated,mitochondrial complex Ⅰ ～Ⅳ activities,reactive oxygen species(ROS) level,malondialdehyde (MDA) content,and total activities of superoxide dismutase (SOD) in the cerebral mitochondria were determined to evaluate the effect of electro-acupuncture at acupoints on anti-oxidative stress of PD mice.Results The motor function of PD mice was improved,the activity of mitochondrial complex Ⅰ was increased,the contents of ROS and MDA in cerebral mitochondria were decreased,and the activity of SOD was increased in the electro-acupuncture group,the differences being significant compared with those of the model group (P ＜ 0.05 or P ＜ 0.01).Conclusion Penetrating electro-acupuncture at scalp-acupoints can increase the anti-oxidative ability of the cerebral mitochondria and improve the motor function of PD mice.

[ ABSTRACT] AIM:To investigate the effect of triptolide on the inhibition of microglial activation in 1-methyl-4-phenyl pyridinium ( MPP+)-induced hemiparkinson disease rats.METHODS:The rat model of Parkinson disease was es-tablished by intranigral injection of MPP +.The rats were randomly divided into sham group, MPP+group, triptolide group and vehicle group.The survival of dopaminergic neurons was detected by the immunofluorescence of tyrosine hydroxylase ( TH) in the substantia nigra ( SN) .The activation of microglia was determined by immunofluorescence of OX-42 ( micro-glia marker) in the SN.The expression of chemokine receptor CX3CR1 in SN was measured by Western blotting.RE-SULTS:Intranigral injection of MPP+increased the fluorescence intensity of the microglial marker, and promoted DA neu-ron degenerative death.Immunohistological analysis showed that the OX-42 density was decreased (P<0.01) and tyrosine hydroxylase (TH) positive neurons were increased in the triptolide group (P<0.01).The expression of CX3CR1 was lower in triptolide group than that in model group (P<0.05).CONCLUSION:Triptolide may improve PA neurons func-tion in MPP+-induced rats through inhibiting CX3CR1 expression and microglial activation.