Ellagic Acid Prevents Dopamine Neuron Degeneration from Oxidative Stress and Neuroinflammation in MPTP Model of Parkinson’s Disease

Autor: Tohru Kitada, M. Emdadul Haque, Greeshma Bharathan, Mustafa T. Ardah
Rok vydání: 2020
Předmět:
Male
0301 basic medicine
lcsh:QR1-502
Nitric Oxide Synthase Type II
Substantia nigra
Pharmacology
Biochemistry
Neuroprotection
lcsh:Microbiology
Article
Lipid peroxidation
Mice
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
ellagic acid
Dopamine
neurotoxicity
medicine
Animals
Molecular Biology
Dopamine transporter
biology
Pars compacta
Dopaminergic Neurons
MPTP
Dopaminergic
neurodegeneration
Parkinson Disease
Glutathione
Corpus Striatum
nervous system diseases
Mice
Inbred C57BL
Disease Models
Animal
Oxidative Stress
Neuroprotective Agents
030104 developmental biology
nervous system
chemistry
1-Methyl-4-phenyl-1
2
3
6-tetrahydropyridine
Parkinson’s disease
biology.protein
Lipid Peroxidation
Inflammation Mediators
030217 neurology & neurosurgery
medicine.drug
Zdroj: Biomolecules
Volume 10
Issue 11
Biomolecules, Vol 10, Iss 1519, p 1519 (2020)
ISSN: 2218-273X
DOI: 10.3390/biom10111519
Popis: Parkinson&rsquo
s disease (PD) is one of the most common neurodegenerative diseases and is characterized by progressive dopaminergic neurodegeneration in the substantia nigra pars compacta area. In the present study, treatment of EA for 1 week at a dose of 10 mg/kg body weight prior to MPTP (25 mg/kg body weight) was carried out. MPTP administration caused oxidative stress, as evidenced by decreased activities of superoxide dismutase and catalase, and the depletion of reduced glutathione with a concomitant rise in the lipid peroxidation product, malondialdehyde. It also significantly increased the pro-inflammatory cytokines and elevated the inflammatory mediators like cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in the striatum. Immunohistochemical analysis revealed a loss of dopamine neurons in the SNc area and a decrease in dopamine transporter in the striatum following MPTP administration. However, treatment with EA prior to MPTP injection significantly rescued the dopaminergic neurons and dopamine transporter. EA treatment further restored antioxidant enzymes, prevented the depletion of glutathione and inhibited lipid peroxidation, in addition to the attenuation of pro-inflammatory cytokines. EA also reduced the levels of COX-2 and iNOS. The findings of the present study demonstrate that EA protects against MPTP-induced PD and the observed neuroprotective effects can be attributed to its potent antioxidant and anti-inflammatory properties.
Databáze: OpenAIRE
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