Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic (DA) neurons at the substantia nigra. Mitochondrial dysfunction is involved in the mechanism of cell damage in Parkinson’s disease (PD). 6-Hydroxydopamine (6-OHDA) is a dopamine analog which specifically damages dopaminergic neurons. Baicalein has been previously reported to have potential in the treatment of PD. The purpose of the present study was to investigate the mechanism of action of baicalein against 6-OHDA injury in SH-SY5Y cells. The results showed that baicalein significantly alleviated alterations of mitochondrial redox activity and mitochondrial membrane potential induced by 6-OHDA in a dose-dependent manner in SH-SY5Y cells compared with vehicle group. Futhermore, baicalein decreased the production of ROS and upregulated the DJ-1 protein expression in SH-SY5Y cells. In addition, baicalein also inhibited ROS production and lipid peroxidation (IC50 = 6.32 ± 0.03 μM) in rat brain mitochondia. In summary, the underlying mechanisms of baicalein against 6-OHDA-induced mitochondrial dysfunction may involve inhibition of mitochondrial oxidation and upregulation of DJ-1 protein expression.
Highlights
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by slowly progressive degeneration of dopamine (DA) neurons in the substantia nigra pars compacta, with subsequent damage of nerve terminals, accompanied by DA depletion in the striatum
It is known that 6-OHDA could selectively cause degeneration of the nigrostriatal dopaminergic neuronal pathway in several animals [22] and cells [34,35], so 6-OHDA-damaged SH-SY5Y cells were used as an in vitro PD model in our studies to investigate the possible mechanism of action of baicalein
Co-treatment with baicalein protected the cells from 6-OHDA damage
Summary
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by slowly progressive degeneration of dopamine (DA) neurons in the substantia nigra pars compacta, with subsequent damage of nerve terminals, accompanied by DA depletion in the striatum. Mitochondrial diseases often have an associated metabolic component, and mitochondrial defects are expected in aging, and other energy-dependent disturbances [7] In such disturbances, cellular oxidative damage caused by the generation of reactive oxygen species (ROS) that exceed the natural antioxidant activity is likely an initiating factor in aging [8]. The SH-SY5Y cell line has become a popular cell model for PD research because this cell line possesses many characateristics of DAergic neurons [23] It has been used as an in vitro model for the study of PD and to determine the effect of protective and therapeutic agents. The 6-OHDA-induced SH-SY5Y cell toxicity was used as a vitro PD model in our studies to investigate the possible protective effect of baicalein. The purpose of this study was to explore the mechanism of action of baicalein against PD
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