Abstract
BackgroundParkinson’s disease (PD) is the second most common neurodegenerative disease, affecting 2% of the population aged over 65 years old. Mitochondrial defects and oxidative stress actively participate in degeneration of dopaminergic (DA) neurons in PD. Paeonolum, a main component isolated from Moutan cortex, has potent antioxidant ability. Here, we have examined the effects of paeonolum against MPP+-induced neurotoxicity in zebrafish and PC12 cells.MethodsThe overall viability and neurodegeneration of DA neurons was assessed in ETvmat2:green fluorescent protein (GFP) transgenic zebrafish, in which most monoaminergic neurons are labeled by GFP. Damage to PC12 cells was measured using a cell viability assay and assessment of nuclear morphology. Intracellular reactive oxygen species (ROS) and the level of total GSH were assessed. The mitochondrial cell death pathway including mitochondrial membrane potential, cytochrome C release and caspase-3 activity were also examined in PC12 cells.ResultsPaeonolum protected against MPP+-induced DA neurodegeneration and locomotor dysfunction in zebrafish in a concentration-dependent manner. Similar neuroprotection was replicated in the PC12 cellular model of MPP+ toxicity. Paeonolum attenuated MPP+-induced intracellular ROS accumulation and restored the level of total GSH in PC12 cells. Furthermore, paeonolum significantly inhibited the mitochondrial cell death pathway induced by MPP+.ConclusionsCollectively, the present study demonstrates that paeonolum protects zebrafish and PC12 cells against MPP+-induced neurotoxicity.
Highlights
Parkinson’s disease (PD) is the second most common neurodegenerative disease, affecting 2% of the population aged over 65 years old
There were no significant morphological alterations observed in larval zebrafish receiving MPP+ up to1000 μM, compared with untreated controls, indicating that MPP+ has no obvious effect on normal embryonic development of zebrafish (Figure 1A)
We further studied whether MPP+ had a specific toxic effect on DA neurons in the ETvmat2:GFP line of zebrafish
Summary
Parkinson’s disease (PD) is the second most common neurodegenerative disease, affecting 2% of the population aged over 65 years old. Mitochondrial defects and oxidative stress actively participate in degeneration of dopaminergic (DA) neurons in PD. A main component isolated from Moutan cortex, has potent antioxidant ability. We have examined the effects of paeonolum against MPP+-induced neurotoxicity in zebrafish and PC12 cells. Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease, affecting 2% of the population aged over 65 years. The pathogenesis of PD remains largely unknown, both oxidative stress and mitochondrial dysfunction play pivotal roles in the pathogenesis of PD. A defect in respiratory chain complex I activity in mitochondria has been observed in dopaminergic (DA) neurons in PD patients [3,4,5,6,7]. The majority of PD cases are sporadic, indicating a critical role for environmental factors in the pathogenesis of PD. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is an environmental toxin and can selectively damage DA neurons in the substantia nigra (SN) which in turn leads
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