Title:Vinpocetine Exerts Neuroprotective Effects via Downregulating α-Syn in Rotenone-induced Cellular Models of Parkinson’s Disease
Volume: 21
Issue: 14
Author(s): Meng Ji*, Ji-Hua Xu, He-Yin Mi, Peng Jiang and Yue Li
Affiliation:
- Department of Neurology, Beijing Chao-yang Hospital, Capital Medical University. Beijing, 100020, China
Keywords:
Parkinson's disease, vinpocetine, α-synuclein, cytotoxicity, dopaminergic, polyvinylidene fluoride.
Abstract:
Objective: Vinpocetine (Vinp), a derivative of alkaloid vincristine with anti-inflammatory
and antioxidant effects, has been shown to have neuroprotective effects in Parkinson's disease (PD).
Its role and mechanisms, however, are not fully understood. Therefore, the aim of this study was to
investigate the effects and possible mechanisms of Vinp on PD cells.
Methods: SH-SY5Y cells were treated with Vinp and then with rotenone to induce a cellular model
of PD. The proliferation level and apoptosis rate of SH-SY5Y cells after different treatments were
detected by MTT and flow cytometry assays, respectively. Western blot was used to determine the
relative protein expression of α-Synuclein (α-Syn) in differently treated cells. Additionally, commercial
kits and ELISA were used to determine oxidative stress-related indicators (superoxide dismutase
(SOD), malondialdehyde (MDA), and reactive oxygen species (ROS)) and inflammatory factors
(tumor necrosis factor α [TNF-α], interleukin-5 (IL-5), and interleukin-1β (IL-1β)) in SH-SY5Y cells
after different treatments, respectively.
Results: Vinp at different concentrations (5, 10, and 50 μM) had no significant effect on the proliferation
and apoptosis of SH-SY5Y cells. For rotenone-induced SH-SY5Y cells, Vinp pretreatment
could significantly reduce α-Syn expression, increased cell viability and decreased apoptosis, oxidative
stress (downregulation of ROS and MDA levels and upregulation of SOD activity) and inflammation
(increased levels of TNF-α, IL-5, and IL-1β). In contrast, overexpression of α-Syn in SHSY5Y
cells with Vinp pretreatment and rotenone induction partially reversed the aforementioned
protective effects of Vinp, causing a decrease in proliferation, an increase in apoptosis rate, inflammation,
and oxidative stress.
Conclusion: Vinp exerted neuroprotective effects by downregulating α-Syn to promote proliferation,
inhibit apoptosis, and inhibit oxidative stress and inflammation in rotenone-induced SH-SY5Y cells.
