Exercise-induced inflammatory responses-reduced a-synuclein aggregation and improve motor function in a transgenic mouse model of Parkinson's disease

摘要

Therefore, EA may represent an effective adjuvant therapy for motor deficits in patients with PD. Corynoxine play a neuroprotection role ona rotenone rat model of Parkinson’s disease Parkinson’s disease (PD), the second most common neu- rodegenerative disorder, is characterized by the accumulation of pathological protein aggregates (namely Lewy bodies) in dopaminergic neurons in the substantianigra region of the brain. Alpha-synuclein (a-syn) is the major component of Lewy bod- ies in PD patients, and impairment of the autophagy-lysosomal pathway is proved to be related to the pathologic development of PD. Therefore, small molecular autophagy enhancers are suggested to be potential drugs for PD treatment. Previously, we identified Corynoxine (Cory), an alkaloid from Chinese herb Gouteng, as a new autophagy enhancer which promotes the degradation of a-syn in a cell model of PD. In this study, we established a rotenone rat model of PD and found that Cory improves the motor dysfunction via increasing dopamine level, prevents neurons loss via increas- ing tyrosine hydroxylase (TH) level, decreases a-syn aggregation via autophagy enhancement and decreases active microglia cells on this model. All these results demonstrate the neuroprotection of Cory on the rotenone rat model of PD, and provides experimen- tal evidences on rat to develop Cory to be potential drug for PD treatment.