Objective To explore the possible mechanism of Tianma Gouteng Yin（ 天麻钩藤饮） in treating Parkinson’s disease. Methods A rat model of Parkinson’ s disease was established by 6-hydroxydopamine injection.After successful model establishment

the rats were randomly divided into model group

western medicine group

and high or low dose groups of traditional Chinese medicine

and a sham operation group

10 rats in each group. The low and high dose groups of traditional Chinese medicine were given Tianma Gouteng Yin 11. 88 and 47. 52 g/（ kg·d）gavage

respectively

and the western medicine group were given tobabasic tablets 75 mg/（ kg·d） gavage. The same amount of saline was given to the the model group and the sham speration group for a total of 8 weeks. HE staining was used to observe the morphological changes of brain tissue in rats. Immunohistochemistry was used to determine the content of α-synuclein in the striatum and the expression of autophagy-related proteins Beclin1 and LC3 B. Results In the sham operation group

the striatum neurons were densely packed and the morphology was normal. In the model group

the damage of the neurons was severe and the number of nerve cells was significantly reduced. The striatum cell morphology of the high

low dose of the Chinese medicine group and western medicine group was improved compared with that of the model group. Compared with the sham group

the gray value of α-synuclein in the striatum of the model group decreased

and the gray value of Beclin1 and LC3 B increased（ P < 0. 05）. Compared with the model group

the gray value of α-synuclein in the high and low dose group as well as the western medicine group increased

and the gray levels of Beclin1 and LC3 B in the high-dose

low-dose group and western medicine group decreased（ P < 0. 05）. Compared with western medicine group

the gray value of α-synuclein in high-dose group was increased

and the gray value of Beclin1 was decreased（ P < 0. 05）. Conclusion Tianma Gouteng Yin may play a neuroprotective role by scavenging excess α-synuclein and upregulating autophagy activity in striatum.