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Abstract
Context: The twigs of Sorbus alnifolia (Sieb. et Zucc.) K. Koch (Rosaceae) have been used to treat neurological disorders as a traditional medicine in Korea. However, there are limited data describing the efficacy of S. alnifolia in Parkinson’s disease (PD). Objective: This study was conducted to identify the protective effects of the methanol extracts of S. alnifolia (MESA) on the dopaminergic (DA) neurodegeneration in Caenorhabditis elegans. Materials and methods: To test the neuroprotective action of MESA, viability assay was performed after 48 h exposure to 1-methyl-4-phenylpyridine (MMP+) in PC12 cells and C. elegans (400 μM and 2 mM of MMP+, respectively). Fluorescence intensity was quantified using transgenic mutants such as BZ555 (Pdat-1::GFP) and and UA57 (Pdat-1::GFP and Pdat-1::CAT-2) to determine MESA’s effects on DA neurodegeneration in C. elegans. Aggregation of α-synuclein was observed using NL5901 strain (unc-54p::α-synuclein::YFP). MESA’s protective effects on the DA neuronal functions were examined by food-sensing assay. Lifespan assay was conducted to test the effects of MESA on the longevity. Results: MESA restored MPP+-induced loss of viability in both PC12 cells and C. elegans (85.8% and 54.9%, respectively). In C. elegans, MESA provided protection against chemically and genetically-induced DA neurodegeneration, respectively. Moreover, food-sensing functions were increased 58.4% by MESA in the DA neuron degraded worms. MESA also prolonged the average lifespan by 25.6%. However, MESA failed to alter α-synuclein aggregation. Discussion and conclusions: These results revealed that MESA protects DA neurodegeneration and recovers diminished DA neuronal functions, thereby can be a valuable candidate for the treatment of PD.
Highlights
Parkinson’s disease (PD) is a major progressive neurodegenerative disorder and the prevalence rate of PD for those aged 65 and above is more than 1% (Dawson & Dawson 2002)
methanol extracts of S. alnifolia (MESA) failed to alter a-synuclein aggregation. These results revealed that MESA protects DA neurodegeneration and recovers diminished DA neuronal functions, thereby can be a valuable candidate for the treatment of PD
The pathogenesis of PD is not completely clear, accumulating evidence suggests that mitochondrial dysfunction results in increased reactive oxygen species (ROS) production and decreased ATP synthesis possibly generate the loss of dopaminergic cells (Trimmer & Bennett 2009)
Summary
Parkinson’s disease (PD) is a major progressive neurodegenerative disorder and the prevalence rate of PD for those aged 65 and above is more than 1% (Dawson & Dawson 2002). The main symptoms of PD are tremor, bradykinesia and rigidity resulting from the death of dopaminergic (DA) neurons in the substantia nigra of the midbrain as well as Lewy body accumulation. The Parkinson’s symptoms can be managed with several medications which regulate dopamine level in the brain or mimic the dopamine effect. To date, there is no available treatment that cures or slows down the progress of this disease. The pathogenesis of PD is not completely clear, accumulating evidence suggests that mitochondrial dysfunction results in increased reactive oxygen species (ROS) production and decreased ATP synthesis possibly generate the loss of dopaminergic cells (Trimmer & Bennett 2009). Preventing mitochondrial dysfunction or reducing oxidative stress has been considered as an attractive therapeutic target for PD treatment
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