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Ellagic Acid Prevents Dopamine Neuron Degeneration from Oxidative Stress and Neuroinflammation in MPTP Model of Parkinson's Disease.
Biomolecules. 2020 11 06; 10(11)B

Abstract

Parkinson'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.

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Authors+Show Affiliations

Ardah MT
Department of Biochemistry, College of Medicine and Health Sciences, UAEU, Al Ain, UAE.
Bharathan G
Department of Biochemistry, College of Medicine and Health Sciences, UAEU, Al Ain, UAE.
Kitada T
Otawa-Kagaku Service, Parkinson's Clinic and Research, Kamakura 247-0061, Japan.
Haque ME
Department of Biochemistry, College of Medicine and Health Sciences, UAEU, Al Ain, UAE.

MeSH

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnimalsCorpus StriatumDisease Models, AnimalDopaminergic NeuronsEllagic AcidGlutathioneInflammation MediatorsLipid PeroxidationMaleMiceMice, Inbred C57BLNeuroprotective AgentsNitric Oxide Synthase Type IIOxidative StressParkinson Disease

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

33172035

Citation

Ardah, Mustafa T., et al. "Ellagic Acid Prevents Dopamine Neuron Degeneration From Oxidative Stress and Neuroinflammation in MPTP Model of Parkinson's Disease." Biomolecules, vol. 10, no. 11, 2020.
Ardah MT, Bharathan G, Kitada T, et al. Ellagic Acid Prevents Dopamine Neuron Degeneration from Oxidative Stress and Neuroinflammation in MPTP Model of Parkinson's Disease. Biomolecules. 2020;10(11).
Ardah, M. T., Bharathan, G., Kitada, T., & Haque, M. E. (2020). Ellagic Acid Prevents Dopamine Neuron Degeneration from Oxidative Stress and Neuroinflammation in MPTP Model of Parkinson's Disease. Biomolecules, 10(11). https://doi.org/10.3390/biom10111519
Ardah MT, et al. Ellagic Acid Prevents Dopamine Neuron Degeneration From Oxidative Stress and Neuroinflammation in MPTP Model of Parkinson's Disease. Biomolecules. 2020 11 6;10(11) PubMed PMID: 33172035.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ellagic Acid Prevents Dopamine Neuron Degeneration from Oxidative Stress and Neuroinflammation in MPTP Model of Parkinson's Disease. AU - Ardah,Mustafa T, AU - Bharathan,Greeshma, AU - Kitada,Tohru, AU - Haque,M Emdadul, Y1 - 2020/11/06/ PY - 2020/09/23/received PY - 2020/10/30/revised PY - 2020/11/04/accepted PY - 2020/11/11/entrez PY - 2020/11/12/pubmed PY - 2021/9/3/medline KW - Parkinson’s disease KW - ellagic acid KW - neurodegeneration KW - neurotoxicity JF - Biomolecules JO - Biomolecules VL - 10 IS - 11 N2 - Parkinson'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. SN - 2218-273X UR - https://www.unboundmedicine.com/medline/citation/33172035/Ellagic_Acid_Prevents_Dopamine_Neuron_Degeneration_from_Oxidative_Stress_and_Neuroinflammation_in_MPTP_Model_of_Parkinson's_Disease_ DB - PRIME DP - Unbound Medicine ER -