Abstract
Mitochondrial dysfunction has been implicated in the pathogenesis of Parkinson’s disease (PD) for several decades, and disturbed mitochondrial biogenesis (mitobiogenesis) was recently found to be a common phenomenon in PD. Baicalein, a major bioactive flavone of Scutellaria baicalensis Georgi, exerted neuroprotective effects in several experimental PD models. However, the effects of baicalein in rotenone-induced PD rats and the possible mechanisms remain poorly understood. In this study, we evaluated the therapeutic effects of baicalein and explored its mechanism of action in rotenone-induced PD models. The results indicated that behavioural impairments and the depletion of dopaminergic neurons induced by rotenone were attenuated by baicalein. Furthermore, in rotenone-induced parkinsonian rats, baicalein treatment effectively restored mitochondrial function and improved mitobiogenesis, as determined by measuring the mitochondrial density and key regulators involved in mitobiogenesis. Additionally, we confirmed that baicalein enhanced mitobiogenesis through the cAMP-responsive element binding protein (CREB) and glycogen synthase kinase-3β (GSK-3β) pathways in rotenone-treated SH-SY5Y cells. Moreover, we demonstrated that the cytoprotective effects of baicalein could be attenuated by the mitobiogenesis inhibitor chloramphenicol as well as CREB siRNA transfection. Overall, our results suggested that baicalein partially enhanced mitobiogenesis to restore mitochondrial function, thus exerting therapeutic effects in rotenone-induced PD models.
Highlights
Parkinson’s disease (PD), the second most common neurodegenerative disease, is characterized by the selective and progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta, which leads to disabling motor abnormalities such as tremor at rest, rigidity, bradykinesia, and postural instability[1, 2]
Baicalein dose-dependently increased the number of tyrosine hydroxylase (TH)+ neurons, with 27.55% more TH+ neurons in rats treated with 200 mg/kg baicalein and 100.30% more TH+ neurons in those treated with 400 mg/kg baicalein compared with that observed in the PD model rats not treated with baicalein (DAY 42) (Fig. 1d,e)
We report a therapeutic effect of baicalein on rotenone-induced PD rats and a novel role of baicalein in restoring mitochondrial function, especially mitobiogenesis
Summary
Parkinson’s disease (PD), the second most common neurodegenerative disease, is characterized by the selective and progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta, which leads to disabling motor abnormalities such as tremor at rest, rigidity, bradykinesia, and postural instability[1, 2]. Results Effects of baicalein on the behavioural impairments and TH-positive cell numbers in the substantia nigra in rotenone-induced PD rats. All of the above results suggested that baicalein partially ameliorated the motor dysfunction and increased the number of TH+ cells in the SN in rotenone-induced PD rats.
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