Vinpocetine improves dyskinesia in Parkinson's disease rats by reducing oxidative stress and activating the Wnt/β-catenin signaling pathway.

Parkinson's disease (PD) is the commonest neurodegenerative disorder. It reduces motor and cognitive function in patients. Vinpocetine (Vinp) has the effects of anti-inflammatory and antioxidant, and could improve cognitive function in patients. This study was aimed to investigating the therapeutic effects of Vinp on dyskinesia in a 6-Hydroxydopamine hydrobromide (6-OHDA)-induced PD rat model. We constructed a PD rat model by injecting 6-OHDA, and intervened with Vinp for 7 days. The motor function of the rats was evaluated by an open-field test and rotation test. Besides, H&E staining was applied to observe the changes of dopaminergic neurons in the striatum. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in the rat striatum were detected. We assessed the impact of Vinp on α-synuclein (α-Syn) and Wnt/β-catenin signaling pathway-related molecules by western blot and qRT-PCR. Rats in the PD group showed reduced horizontal movement frequency and number of squares crossed, increased contact time and rotation frequency, and reduced number of dopaminergic neurons accompanied by severe morphological damage. Vinp treatment increased the horizontal movement frequency and number of squares crossed, reduced the contact time, and rotation frequency in PD rats. Also, Vinp downregulated α-Syn protein expression and MDA level, while upregulated SOD activity in the striatum of PD rats. Furthermore, Vinp treatment activated the Wnt/β-catenin signaling pathway in the striatum of PD rats. In conclusion, Vinp improved the dyskinesia in 6-OHDA-induced PD rats by alleviating oxidative stress, and these effects may be associated with activating the Wnt/β-catenin signaling pathway.