Abstract
This research assessed the molecular mechanism of procyanidins (PCs) against neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its metabolite 1-methyl-4-phenylpyridinium (MPP+) induced Parkinson’s disease (PD) models. In vitro, PC12 cells were incubated with PCs or deprenyl for 24 h, and then exposed to 1.5 mM MPP+ for 24 h. In vivo, zebrafish larvae (AB strain) 3 days post-fertilization (dpf) were incubated with deprenyl or PCs in 400 μM MPTP for 4 days. Compared with MPP+/MPTP alone, PCs significantly improved antioxidant activities (e.g., glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT)), and decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Furthermore, PCs significantly increased nuclear Nrf2 accumulation in PC12 cells and raised the expression of NQO1, HO-1, GCLM, and GCLC in both PC12 cells and zebrafish compared to MPP+/MPTP alone. The current study shows that PCs have neuroprotective effects, activate the nuclear factor-erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway and alleviate oxidative damage in MPP+/MPTP-induced PD models.
Highlights
Parkinson’s disease (PD) is a progressive neurodegenerative syndrome caused by the absence of dopaminergic neurons in the substantia nigra
Dopamine can undergo auto- or enzyme-catalyzed oxidation to lead the production of reactive oxygen species (ROS) and electrophilic quinone molecules [9], both processes that may underlie the vulnerability of dopaminergic neurons to oxidative and electrophilic stress [10,11,12]
ROS and malondialdehyde (MDA) levels indicate the severity of oxidative damage
Summary
Parkinson’s disease (PD) is a progressive neurodegenerative syndrome caused by the absence of dopaminergic neurons in the substantia nigra. Effective methods to prevent or reverse neuronal degeneration in PD patients are still unclear. The pathogenesis of PD remains unclear, previous studies have demonstrated that oxidative stress plays a key role in the loss of dopaminergic neurons [7,8]. Dopamine can undergo auto- or enzyme-catalyzed oxidation to lead the production of reactive oxygen species (ROS) and electrophilic quinone molecules [9], both processes that may underlie the vulnerability of dopaminergic neurons to oxidative and electrophilic stress [10,11,12]. A possible method for the prevention or treatment of PD may be to supplement treatment with antioxidants to eliminate excessive ROS. Antioxidant compounds from natural resources may aid in the treatment of PD
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