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      Is Open Access

      Beneficial effects of L-arginine on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neuronal degeneration in substantia nigra of Balb/c mice

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          Abstract

          Background:

          L-arginine has been recently investigated and proposed to reduce neurological damage after various experimental models of neuronal cellular damage. In this study, we aim to evaluate the beneficial effects of L-arginine administration on the numerical density of dark neurons (DNs) in the substantia nigra pars compacta (SNc) of Balb/c mice subjected to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration.

          Materials and Methods:

          Male Balb/c mice were randomly divided into 4 groups ( n = 7 each): MPTP only; saline only (control); MPTP + L-arginine; and L-arginine only. The animals were infused intranasally with a single intranasal administration of the proneurotoxin MPTP (1 mg/nostril). L-arginine (300 mg/kg) was administrated intraperitoneally once daily for 1-week starting from 3 days after MPTP administration. Cavalieri principle method was used to estimate the numerical density of DNs in the SNc of different studied groups.

          Results:

          Twenty days following MPTP administration, the number of DNs was significantly increased when compared to sham-control and L-arginine-control groups ( P < 0.05). Nevertheless, our results showed that L-arginine administration significantly decreased the numerical density of DNs in SNc of mice.

          Conclusion:

          This investigation provides new insights in experimental models of Parkinson’s disease, indicating that L-arginine represents a potential treatment agent for dopaminergic neuron degeneration in SNc observed in Parkinson’s disease patients.

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          Most cited references56

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          • Abstract: found
          • Article: found

          Etiology and pathogenesis of Parkinson's disease.

          The past 25 years have seen a major expansion of knowledge concerning the cause of Parkinson's disease provided by an understanding of environmental and genetic factors that underlie the loss of nigral dopaminergic neurons. Based on the actions of toxins, postmortem investigations, and gene defects responsible for familial Parkinson's disease, there is now a general consensus about the mechanisms of cell death that contribute to neuronal loss in Parkinson's disease. Mitochondrial dysfunction, oxidative stress, altered protein handling, and inflammatory change are considered to lead to cell dysfunction and death by apoptosis or autophagy. Ageing is the single most important risk factor for Parkinson's disease, and the biochemical changes that are a consequence of aging amplify these abnormalities in Parkinson's disease brain. What remains to be determined is the combination and sequence of events leading to cell death and whether this is identical in all brain regions where pathology occurs and in all individuals with Parkinson's disease. Focusing on those events that characterize Parkinson's disease, namely, mitochondrial dysfunction and Lewy body formation, may be the key to further advancing the understanding of pathogenesis and to taking these mechanisms forward as a means of defining targets for neuroprotection. Copyright © 2011 Movement Disorder Society.
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            Nitric oxide signaling in the central nervous system.

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              Epidemiology of Parkinson's disease.

              Epidemiological research aims to provide information on the development, prevalence and progression of diseases, and their associated risk factors. Epidemiological research is thus the basis of increasing our understanding on the aetiology of diseases and as a consequence the starting point for identifying at risk groups in the population, development for novel prevention and treatment strategies, and health care planning. This review provides an overview of the epidemiology of Parkinson's disease, the second most common neurodegenerative disorder, with special emphasis on population-based data on the clinical progression of motor and non-motor features of the disease.
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                Author and article information

                Journal
                Adv Biomed Res
                Adv Biomed Res
                ABR
                Advanced Biomedical Research
                Medknow Publications & Media Pvt Ltd (India )
                2277-9175
                2016
                30 August 2016
                : 5
                : 140
                Affiliations
                [1]Department of Anatomical Sciences, School of Medicine, Birjand University of Medical Sciences, Birjand, Iran
                [1 ]Department of Public Health, Research Centre of Experimental Medicine, Deputy of Research and Technology, Birjand University of Medical Sciences, Birjand, Iran
                [2 ]Department of Biology, School of Sciences, Payam-e-Noor University, Tehran, Iran
                [3 ]Student of Medicine, Department of Anatomical Sciences, School of Medicine, Birjand University of Medical Sciences, Birjand, Iran
                [4 ]Department of Anatomical Sciences and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                Author notes
                Address for correspondence: Dr. Akram Sadeghi, Department of Anatomical Sciences, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. E-mail: akramsdg62@ 123456yahoo.com
                Article
                ABR-5-140
                10.4103/2277-9175.187374
                5025923
                2cb4ef80-d5fe-4a8e-8e63-07b40da2579f
                Copyright: © 2016 Advanced Biomedical Research

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

                History
                : 18 August 2015
                : 09 September 2015
                Categories
                Original Article

                Molecular medicine
                1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine,balb/c mice,l-arginine,substantia nigra
                Molecular medicine
                1-methyl-4-phenyl-1, 2, 3, 6 tetrahydropyridine, balb/c mice, l-arginine, substantia nigra

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