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Antioxidants
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The Role of Natural Antioxidant in the Treatment of Neurological...
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The Role of Natural Antioxidant in the Treatment of Neurological Disorders

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 12139

Special Issue Editor

Dr. Sunoh Kim

E-Mail Website
Guest Editor
Central R&D Center, B&Tech Co., Ltd., Gwangju, Republic of Korea
Interests: electroneurophysiology; neuroreceptors; voltage-dependent calcium channels; neurological diseases; cardiovascular disease; neuropharmacology; molecular biology; natural product; Alzheimer’s disease; obesity; hypertension
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The nervous system plays an important role in the functioning of animals, and is involved in diverse functions, including sight, touch, smell, memory, and emotion control. This system is composed of various neuronal and non-neuronal cells that perfectly control the processes that occur in an animal’s body. To date, many studies have reported the discovery new drugs that inhibit neuronal cell death and regenerate neuronal cells. However, these drugs are limited in their ability to treat many neurological diseases, including dementia and depression. In this Special Issue, we aim to examine the application of natural products to the control of various neurological disorders. Researchers must aim to discover natural products with potential for treating central and peripheral nervous system diseases and discuss their applicability as therapeutic agents. Natural products contain various phytochemicals, the diversity of which could suggest their multi-functional potential; thus, their antioxidant effects should be discussed. It is important that researchers seek natural product-based therapeutic approaches to diseases that occur in nerve cells and the nervous system, including in the cerebral, optic, sensory, and olfactory nerves. We encourage authors to submit research on the treatment of neurological diseases using natural products. 

Topics include, but are not limited to, the following:

  • Mechanism of optic nerve damage caused by glaucoma;
  • The discovery of new drugs that modulate excitatory neurotransmitter receptors;
  • The discovery of new drugs that modulate inhibitory neurotransmitter receptors;
  • The discovery of new drugs that regulate ion channels;
  • The discovery of pain control drugs;
  • The discovery of new drugs for Alzheimer's disease;
  • The discovery of new drugs for depression;
  • Novel mechanisms of nervous system injury.

Dr. Sunoh Kim
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • phytochemicals
  • nervous system
  • neuronal cell death
  • neurological diseases
  • dementia
  • depression

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Published Papers (4 papers)

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Research

19 pages, 6802 KiB  
Article
Resveratrol Activates Antioxidant Protective Mechanisms in Cellular Models of Alzheimer’s Disease Inflammation
by Clara Bartra, Yi Yuan, Kristijan Vuraić, Haydeé Valdés-Quiroz, Pau Garcia-Baucells, Mark Slevin, Ylenia Pastorello, Cristina Suñol and Coral Sanfeliu
Antioxidants 2024, 13(2), 177; https://doi.org/10.3390/antiox13020177 - 31 Jan 2024
Cited by 20 | Viewed by 4389
Abstract
Resveratrol is a natural phenolic compound with known benefits against neurodegeneration. We analyzed in vitro the protective mechanisms of resveratrol against the proinflammatory monomeric C-reactive protein (mCRP). mCRP increases the risk of AD after stroke and we previously demonstrated that intracerebral mCRP induces [...] Read more.
Resveratrol is a natural phenolic compound with known benefits against neurodegeneration. We analyzed in vitro the protective mechanisms of resveratrol against the proinflammatory monomeric C-reactive protein (mCRP). mCRP increases the risk of AD after stroke and we previously demonstrated that intracerebral mCRP induces AD-like dementia in mice. Here, we used BV2 microglia treated with mCRP for 24 h in the presence or absence of resveratrol. Cells and conditioned media were collected for analysis. Lipopolysaccharide (LPS) has also been implicated in AD progression and so LPS was used as a resveratrol-sensitive reference agent. mCRP at the concentration of 50 µg/mL activated the nitric oxide pathway and the NLRP3 inflammasome pathway. Furthermore, mCRP induced cyclooxygenase-2 and the release of proinflammatory cytokines. Resveratrol effectively inhibited these changes and increased the expression of the antioxidant enzyme genes Cat and Sod2. As central mechanisms of defense, resveratrol activated the hub genes Sirt1 and Nfe2l2 and inhibited the nuclear translocation of the signal transducer NF-ĸB. Proinflammatory changes induced by mCRP in primary mixed glial cultures were also protected by resveratrol. This work provides a mechanistic insight into the protective benefits of resveratrol in preventing the risk of AD induced by proinflammatory agents. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidant in the Treatment of Neurological Disorders)
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18 pages, 4156 KiB  
Article
Pectolinarigenin Improves Oxidative Stress and Apoptosis in Mouse NSC-34 Motor Neuron Cell Lines Induced by C9-ALS-Associated Proline–Arginine Dipeptide Repeat Proteins by Enhancing Mitochondrial Fusion Mediated via the SIRT3/OPA1 Axis
by Ru-Huei Fu
Antioxidants 2023, 12(11), 2008; https://doi.org/10.3390/antiox12112008 - 16 Nov 2023
Cited by 6 | Viewed by 2248
Abstract
Amyotrophic lateral sclerosis (ALS) is considered a fatal progressive degeneration of motor neurons (MN) caused by oxidative stress and mitochondrial dysfunction. There are currently no treatments available. The most common inherited form of ALS is the C9orf72 mutation (C9-ALS). The proline–arginine dipeptide repeat [...] Read more.
Amyotrophic lateral sclerosis (ALS) is considered a fatal progressive degeneration of motor neurons (MN) caused by oxidative stress and mitochondrial dysfunction. There are currently no treatments available. The most common inherited form of ALS is the C9orf72 mutation (C9-ALS). The proline–arginine dipeptide repeat protein (PR-DPR) produced by C9-ALS has been confirmed to be a functionally acquired pathogenic factor that can cause increased ROS, mitochondrial defects, and apoptosis in motor neurons. Pectolinarigenin (PLG) from the traditional medicinal herb Linaria vulgaris has antioxidant and anti-apoptotic properties. I established a mouse NSC-34 motor neuron cell line model expressing PR-DPR and confirmed the neuroprotective effect of PLG. The results showed that ROS production and apoptosis caused by PR-DPR could be improved by PLG treatment. In terms of mechanism research, PR-DPR inhibited the activity of the mitochondrial fusion proteins OPA1 and mitofusin 2. Conversely, the expression of fission protein fission 1 and dynamin-related protein 1 (DRP1) increased. However, PLG treatment reversed these effects. Furthermore, I found that PLG increased the expression and deacetylation of OPA1. Deacetylation of OPA1 enhances mitochondrial fusion and resistance to apoptosis. Finally, transfection with Sirt3 small interfering RNA abolished the neuroprotective effects of PLG. In summary, the mechanism by which PLG alleviates PR-DPR toxicity is mainly achieved by activating the SIRT3/OPA1 axis to regulate the balance of mitochondrial dynamics. Taken together, the potential of PLG in preclinical studies for C9-ALS drug development deserves further evaluation. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidant in the Treatment of Neurological Disorders)
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18 pages, 5940 KiB  
Article
Effects of Dendropanax morbiferus Leaf Extract on Sleep Parameters in Invertebrate and Vertebrate Models
by Kayoung Ko, Yejin Ahn, Ga Yeong Cheon, Hyung Joo Suh, Yun Jae Cho, Sung-Soo Park and Ki-Bae Hong
Antioxidants 2023, 12(10), 1890; https://doi.org/10.3390/antiox12101890 - 21 Oct 2023
Viewed by 2545
Abstract
Dendropanax morbiferus is highly valued in traditional medicine and has been used to alleviate the symptoms of numerous diseases owing to its excellent antioxidant activity. This study aimed to evaluate the sleep promotion and related signaling pathways of D. morbiferus extract (DE) [...] Read more.
Dendropanax morbiferus is highly valued in traditional medicine and has been used to alleviate the symptoms of numerous diseases owing to its excellent antioxidant activity. This study aimed to evaluate the sleep promotion and related signaling pathways of D. morbiferus extract (DE) via behavioral analysis, molecular biological techniques, and electrophysiological measurements in invertebrate and vertebrate models. In Drosophila, the group treated with 4% DE experienced decreased subjective nighttime movement and sleep bout and increased total sleeping time. Moreover, substantial changes in locomotor activity, including distance moved, velocity, and movement, were confirmed in the 4% DE-treated group. Compared to Drosophila in which insomnia and oxidative stress were induced by exposure to 0.1% caffeine, the DE-treated group improved sleep-related parameters to the level of the normal group. In the Drosophila model, exposure to 4% DE upregulated the expression of gamma-aminobutyric acid (GABA)-related receptors and serotonin receptor (5-HT1A), along with the expression of antioxidant-related factors, glutathione, and catalase. In the pentobarbital-induced sleep test using ICR mice, the duration of sleep was markedly increased by high concentration of DE. In addition, through the electroencephalography analysis of SD-rats, a significant increase in non-rapid-eye-movement sleep and delta waves was confirmed with high concentrations of DE administration. The increase in sleep time and improvement in sleep quality were confirmed to be related to the expression of altered GABA receptors and the enhancement of the contents of the neurotransmitters GABA and serotonin (5-HT) because of high DE administration. High-dose administration of DE also increased the expression of antioxidant-related factors in the brain and significantly decreased malondialdehyde content. Taken together, DE induced improvements in sleep quantity and quality by regulating neurotransmitter content and related receptor expression, along with high antioxidant activity, and may have a therapeutic effect on sleep disorders. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidant in the Treatment of Neurological Disorders)
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27 pages, 10202 KiB  
Article
Chiisanoside Mediates the Parkin/ZNF746/PGC-1α Axis by Downregulating MiR-181a to Improve Mitochondrial Biogenesis in 6-OHDA-Caused Neurotoxicity Models In Vitro and In Vivo: Suggestions for Prevention of Parkinson’s Disease
by Yu-Ling Hsu, Hui-Jye Chen, Jia-Xin Gao, Ming-Yang Yang and Ru-Huei Fu
Antioxidants 2023, 12(9), 1782; https://doi.org/10.3390/antiox12091782 - 20 Sep 2023
Cited by 3 | Viewed by 2261
Abstract
The degeneration of dopamine (DA) neurons is known to be associated with defects in mitochondrial biogenesis caused by aging, environmental factors, or mutations in genes, leading to Parkinson’s disease (PD). As PD has not yet been successfully cured, the strategy of using small [...] Read more.
The degeneration of dopamine (DA) neurons is known to be associated with defects in mitochondrial biogenesis caused by aging, environmental factors, or mutations in genes, leading to Parkinson’s disease (PD). As PD has not yet been successfully cured, the strategy of using small molecule drugs to protect and restore mitochondrial biogenesis is a promising direction. This study evaluated the efficacy of synthetic chiisanoside (CSS) identified in the leaves of Acanthopanax sessiliflorus to prevent PD symptoms. The results show that in the 6-hydroxydopamine (6-OHDA) model, CSS pretreatment can effectively alleviate the reactive oxygen species generation and apoptosis of SH-SY5Y cells, thereby lessening the defects in the C. elegans model including DA neuron degeneration, dopamine-mediated food sensitivity behavioral disorders, and shortened lifespan. Mechanistically, we found that CSS could restore the expression of proliferator-activated receptor gamma coactivator-1-alpha (PGC-1α), a key molecule in mitochondrial biogenesis, and its downstream related genes inhibited by 6-OHDA. We further confirmed that this is due to the enhanced activity of parkin leading to the ubiquitination and degradation of PGC-1α inhibitor protein Zinc finger protein 746 (ZNF746). Parkin siRNA treatment abolished this effect of CSS. Furthermore, we found that CSS inhibited 6-OHDA-induced expression of miR-181a, which targets parkin. The CSS’s ability to reverse the 6-OHDA-induced reduction in mitochondrial biogenesis and activation of apoptosis was abolished after the transfection of anti-miR-181a and miR-181a mimics. Therefore, the neuroprotective effect of CSS mainly promotes mitochondrial biogenesis by regulating the miR-181a/Parkin/ZNF746/PGC-1α axis. CSS potentially has the opportunity to be developed into PD prevention agents. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidant in the Treatment of Neurological Disorders)
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