Abstract
Reactive nitrogen species (RNS) and reactive oxygen species (ROS), collectively known as reactive oxygen and nitrogen species (RONS), are the products of normal cellular metabolism and interact with several vital biomolecules including nucleic acid, proteins, and membrane lipids and alter their function in an irreversible manner which can lead to cell death. There is an imperative role for oxidative stress in the pathogenesis of cognitive impairments and the development and progression of neural injury. Elevated production of higher amounts of nitric oxide (NO) takes place in numerous pathological conditions, such as neurodegenerative diseases, inflammation, and ischemia, which occur concurrently with elevated nitrosative/oxidative stress. The enzyme nitric oxide synthase (NOS) is responsible for the generation of NO in different cells by conversion of Larginine (Arg) to L-citrulline. Therefore, the NO signaling pathway represents a viable therapeutic target. Naturally occurring polyphenols targeting the NO signaling pathway can be of major importance in the field of neurodegeneration and related complications. Here, we comprehensively review the importance of NO and its production in the human body and afterwards highlight the importance of various natural products along with their mechanisms against various neurodegenerative diseases involving their effect on NO production.
Keywords: Alzheimer’s, NO, iNOS, neuroinflammation, neurotransmission, neurotoxicity.
Graphical Abstract
Current Neuropharmacology
Title:Role of Nitric Oxide in Neurodegeneration: Function, Regulation, and Inhibition
Volume: 19 Issue: 2
Author(s): Devesh Tewari*, Archana N. Sah, Sweta Bawari, Seyed F. Nabavi, Ahmad R. Dehpour, Samira Shirooie, Nady Braidy, Bernd L. Fiebich, Rosa A. Vacca*Seyed M. Nabavi*
Affiliation:
- Department of Pharmacognosy, School of Pharmaceutical Sciences, Lovely Professional University, Phagwara, Punjab, 144411,India
- Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies, National Council of Research, Bari,Italy
- Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran 1435916471,Iran
Keywords: Alzheimer’s, NO, iNOS, neuroinflammation, neurotransmission, neurotoxicity.
Abstract: Reactive nitrogen species (RNS) and reactive oxygen species (ROS), collectively known as reactive oxygen and nitrogen species (RONS), are the products of normal cellular metabolism and interact with several vital biomolecules including nucleic acid, proteins, and membrane lipids and alter their function in an irreversible manner which can lead to cell death. There is an imperative role for oxidative stress in the pathogenesis of cognitive impairments and the development and progression of neural injury. Elevated production of higher amounts of nitric oxide (NO) takes place in numerous pathological conditions, such as neurodegenerative diseases, inflammation, and ischemia, which occur concurrently with elevated nitrosative/oxidative stress. The enzyme nitric oxide synthase (NOS) is responsible for the generation of NO in different cells by conversion of Larginine (Arg) to L-citrulline. Therefore, the NO signaling pathway represents a viable therapeutic target. Naturally occurring polyphenols targeting the NO signaling pathway can be of major importance in the field of neurodegeneration and related complications. Here, we comprehensively review the importance of NO and its production in the human body and afterwards highlight the importance of various natural products along with their mechanisms against various neurodegenerative diseases involving their effect on NO production.
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Cite this article as:
Tewari Devesh *, Sah N. Archana , Bawari Sweta , Nabavi F. Seyed , Dehpour R. Ahmad , Shirooie Samira , Braidy Nady , Fiebich L. Bernd , Vacca A. Rosa *, Nabavi M. Seyed *, Role of Nitric Oxide in Neurodegeneration: Function, Regulation, and Inhibition, Current Neuropharmacology 2021; 19 (2) . https://dx.doi.org/10.2174/1570159X18666200429001549
DOI https://dx.doi.org/10.2174/1570159X18666200429001549 |
Print ISSN 1570-159X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |

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