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Role of Bioactive Molecules on Neuroprotection, Oxidative Stress and Neuroinflammation...
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Role of Bioactive Molecules on Neuroprotection, Oxidative Stress and Neuroinflammation Modulation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 19107

Special Issue Editors

Dr. Valentina Di Liberto

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Guest Editor
Dipartmento di Biomedicina, Neuroscienze e Diagnostica avanzata (BIND), Università degli Studi di Palermo, Palermo, Italy
Interests: neuroscience; neurotrophic factors; synaptic plasticity; neurodegenerative disease; oxidative stress; neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Giuseppa Mudò

E-Mail Website1 Website2
Guest Editor
Dipartmento di Biomedicina, Neuroscienze e Diagnostica avanzata (BIND), Università degli Studi di Palermo, Palermo, Italy
Interests: neurotrophic factors; synaptic plasticity; neurodegenerative diseases; oxidative stress; neuroinflammation; heteroreceptor complexes; guanosine; epilepsy

Special Issue Information

Dear Colleagues,

A large body of data has demonstrated a strong association between neurodegenerative diseases and extensive oxidative stress and neuroinflammation in the brain. Indeed, the two processes participate in a vicious cycle related to neuronal damage and death. Interestingly, oxidative damage and neuroinflammation seem to occur in the very early stage of the disease and prior to the full development of the pathology. In this context, preventing oxidative stress and neuroinflammation, beyond representing essential pathological biomarkers in neurodegenerative diseases, can serve as therapeutic targets.

For these reasons, this Special Issue aims to identify bioactive molecules for the prevention and treatment of neurodegenerative diseases through the modulation of neuroprotection-, oxidative stress- and neuroinflammation-related signalling pathways, in vitro or in vivo. We invite you to contribute your current work to this Special Issue as an original research or review article, or a short communication.

We look forward to your contributions.

Dr. Valentina Di Liberto
Prof. Dr. Giuseppa Mudò
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neurodegenerative disease
  • neurodegeneration
  • reactive oxygen and nitrogen species
  • mitochondrial dysfunction
  • microglia
  • neurons

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Published Papers (6 papers)

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Editorial

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3 pages, 203 KiB  
Editorial
Role of Bioactive Molecules on Neuroprotection, Oxidative Stress, and Neuroinflammation Modulation
by Valentina Di Liberto and Giuseppa Mudò
Int. J. Mol. Sci. 2022, 23(24), 15925; https://doi.org/10.3390/ijms232415925 - 14 Dec 2022
Cited by 4 | Viewed by 1507
Abstract
As the global population ages, the burden of neurodegenerative and neurological disorders is dramatically increasing [...] Full article
(This article belongs to the Special Issue Role of Bioactive Molecules on Neuroprotection, Oxidative Stress and Neuroinflammation Modulation)

Research

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25 pages, 5356 KiB  
Article
Targeting PSEN1 by lnc-CYP3A43-2/miR-29b-2-5p to Reduce β Amyloid Plaque Formation and Improve Cognition Function
by Wei Wuli, Shinn-Zong Lin, Shee-Ping Chen, Bakhos A. Tannous, Wen-Sheng Huang, Peng Yeong Woon, Yang-Chang Wu, Hsueh-Hui Yang, Yi-Cheng Chen, Renata Lopes Fleming, Jack T. Rogers, Catherine M. Cahill, Tsung-Jung Ho, Tzyy-Wen Chiou and Horng-Jyh Harn
Int. J. Mol. Sci. 2022, 23(18), 10554; https://doi.org/10.3390/ijms231810554 - 11 Sep 2022
Cited by 14 | Viewed by 3347
Abstract
Presenilin-1 (PSEN1) is a crucial subunit within the γ-secretase complex and regulates β-amyloid (Aβ) production. Accumulated evidence indicates that n-butylidenephthalide (BP) acts effectively to reduce Aβ levels in neuronal cells that are derived from trisomy 21 (Ts21) induced pluripotent stem cells [...] Read more.
Presenilin-1 (PSEN1) is a crucial subunit within the γ-secretase complex and regulates β-amyloid (Aβ) production. Accumulated evidence indicates that n-butylidenephthalide (BP) acts effectively to reduce Aβ levels in neuronal cells that are derived from trisomy 21 (Ts21) induced pluripotent stem cells (iPSCs). However, the mechanism underlying this effect remains unclear. This article aims to investigate the possible mechanisms through which BP ameliorates the development of Alzheimer’s disease (AD) and verify the effectiveness of BP through animal experiments. Results from RNA microarray analysis showed that BP treatment in Ts21 iPSC-derived neuronal cells reduced long noncoding RNA (lncRNA) CYP3A43-2 levels and increased microRNA (miR)-29b-2-5p levels. Bioinformatics tool prediction analysis, biotin-labeled miR-29b-2-5p pull-down assay, and dual-luciferase reporter assay confirmed a direct negative regulatory effect for miRNA29b-2-5p on lnc-RNA-CYP3A43-2 and PSEN1. Moreover, BP administration improved short-term memory and significantly reduced Aβ accumulation in the hippocampus and cortex of 3xTg-AD mice but failed in miR-29b-2-5p mutant mice generated by CRISP/Cas9 technology. In addition, analysis of brain samples from patients with AD showed a decrease in microRNA-29b-2-5p expression in the frontal cortex region. Our results provide evidence that the LncCYP3A43-2/miR29-2-5p/PSEN1 network might be involved in the molecular mechanisms underlying BP-induced Aβ reduction. Full article
(This article belongs to the Special Issue Role of Bioactive Molecules on Neuroprotection, Oxidative Stress and Neuroinflammation Modulation)
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17 pages, 3103 KiB  
Article
A Set of Dysregulated Target Genes to Reduce Neuroinflammation at Molecular Level
by Marcella Massimini, Benedetta Bachetti, Elena Dalle Vedove, Alessia Benvenga, Francesco Di Pierro and Nicola Bernabò
Int. J. Mol. Sci. 2022, 23(13), 7175; https://doi.org/10.3390/ijms23137175 - 28 Jun 2022
Cited by 2 | Viewed by 2360
Abstract
Increasing evidence links chronic neurodegenerative diseases with neuroinflammation; it is known that neuroprotective agents are capable of modulating the inflammatory processes, that occur with the onset of neurodegeneration pathologies. Here, with the intention of providing a means for active compounds’ screening, a dysregulation [...] Read more.
Increasing evidence links chronic neurodegenerative diseases with neuroinflammation; it is known that neuroprotective agents are capable of modulating the inflammatory processes, that occur with the onset of neurodegeneration pathologies. Here, with the intention of providing a means for active compounds’ screening, a dysregulation of neuronal inflammatory marker genes was induced and subjected to neuroprotective active principles, with the aim of selecting a set of inflammatory marker genes linked to neurodegenerative diseases. Considering the important role of microglia in neurodegeneration, a murine co-culture of hippocampal cells and inflamed microglia cells was set up. The evaluation of differentially expressed genes and subsequent in silico analysis showed the main dysregulated genes in both cells and the principal inflammatory processes involved in the model. Among the identified genes, a well-defined set was chosen, selecting those in which a role in human neurodegenerative progression in vivo was already defined in literature, matched with the rate of prediction derived from the Principal Component Analysis (PCA) of in vitro treatment-affected genes variation. The obtained panel of dysregulated target genes, including Cxcl9 (Chemokine (C-X-C motif) ligand 9), C4b (Complement Component 4B), Stc1 (Stanniocalcin 1), Abcb1a (ATP Binding Cassette Subfamily B Member 1), Hp (Haptoglobin) and Adm (Adrenomedullin), can be considered an in vitro tool to select old and new active compounds directed to neuroinflammation. Full article
(This article belongs to the Special Issue Role of Bioactive Molecules on Neuroprotection, Oxidative Stress and Neuroinflammation Modulation)
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13 pages, 2621 KiB  
Article
Protective, Antioxidant and Antiproliferative Activity of Grapefruit IntegroPectin on SH-SY5Y Cells
by Domenico Nuzzo, Miriana Scordino, Antonino Scurria, Costanza Giardina, Francesco Giordano, Francesco Meneguzzo, Giuseppa Mudò, Mario Pagliaro, Pasquale Picone, Alessandro Attanzio, Stefania Raimondo, Rosaria Ciriminna and Valentina Di Liberto
Int. J. Mol. Sci. 2021, 22(17), 9368; https://doi.org/10.3390/ijms22179368 - 29 Aug 2021
Cited by 16 | Viewed by 4359
Abstract
Tested in vitro on SH-SY5Y neuroblastoma cells, grapefruit IntegroPectin is a powerful protective, antioxidant and antiproliferative agent. The strong antioxidant properties of this new citrus pectin, and its ability to preserve mitochondrial membrane potential and morphology, severely impaired in neurodegenerative disorders, make it [...] Read more.
Tested in vitro on SH-SY5Y neuroblastoma cells, grapefruit IntegroPectin is a powerful protective, antioxidant and antiproliferative agent. The strong antioxidant properties of this new citrus pectin, and its ability to preserve mitochondrial membrane potential and morphology, severely impaired in neurodegenerative disorders, make it an attractive therapeutic and preventive agent for the treatment of oxidative stress-associated brain disorders. Similarly, the ability of this pectic polymer rich in RG-I regions, as well as in naringin, linalool, linalool oxide and limonene adsorbed at the outer surface, to inhibit cell proliferation or even kill, at high doses, neoplastic cells may have opened up new therapeutic strategies in cancer research. In order to take full advantage of its vast therapeutic and preventive potential, detailed studies of the molecular mechanism involved in the antiproliferative and neuroprotective of this IntegroPectin are urgently needed. Full article
(This article belongs to the Special Issue Role of Bioactive Molecules on Neuroprotection, Oxidative Stress and Neuroinflammation Modulation)
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24 pages, 39190 KiB  
Article
Mechanisms Underlying the Protective Effect of the Peroxiredoxin-6 Are Mediated via the Protection of Astrocytes during Ischemia/Reoxygenation
by Egor A. Turovsky, Elena G. Varlamova and Egor Y. Plotnikov
Int. J. Mol. Sci. 2021, 22(16), 8805; https://doi.org/10.3390/ijms22168805 - 16 Aug 2021
Cited by 25 | Viewed by 3434
Abstract
Ischemia-like conditions reflect almost the entire spectrum of events that occur during cerebral ischemia, including the induction of oxidative stress, Ca2+ overload, glutamate excitotoxicity, and activation of necrosis and apoptosis in brain cells. Mechanisms for the protective effects of the antioxidant enzyme [...] Read more.
Ischemia-like conditions reflect almost the entire spectrum of events that occur during cerebral ischemia, including the induction of oxidative stress, Ca2+ overload, glutamate excitotoxicity, and activation of necrosis and apoptosis in brain cells. Mechanisms for the protective effects of the antioxidant enzyme peroxiredoxin-6 (Prx-6) on hippocampal cells during oxygen-glucose deprivation/reoxygenation (OGD/R) were investigated. Using the methods of fluorescence microscopy, inhibitory analysis, vitality tests and PCR, it was shown that 24-h incubation of mixed hippocampal cell cultures with Prx-6 does not affect the generation of a reversible phase of a OGD-induced rise in Ca2+ ions in cytosol ([Ca2+]i), but inhibits a global increase in [Ca2+]i in astrocytes completely and in neurons by 70%. In addition, after 40 min of OGD, cell necrosis is suppressed, especially in the astrocyte population. This effect is associated with the complex action of Prx-6 on neuroglial networks. As an antioxidant, Prx-6 has a more pronounced and astrocyte-directed effect, compared to the exogenous antioxidant vitamin E (Vit E). Prx-6 inhibits ROS production in mitochondria by increasing the antioxidant capacity of cells and altering the expression of genes encoding redox status proteins. Due to the close bond between [Ca2+]i and intracellular ROS, this effect of Prx-6 is one of its protective mechanisms. Moreover, Prx-6 effectively suppresses not only necrosis, but also apoptosis during OGD and reoxygenation. Incubation with Prx-6 leads to activation of the basic expression of genes encoding protective kinases—PI3K, CaMKII, PKC, anti-apoptotic proteins—Stat3 and Bcl-2, while inhibiting the expression of signaling kinases and factors involved in apoptosis activation—Ikk, Src, NF-κb, Caspase-3, p53, Fas, etc. This effect on the basic expression of the genome leads to the cell preconditions, which is expressed in the inhibition of caspase-3 during OGD/reoxygenation. A significant effect of Prx-6 is directed on suppression of the level of pro-inflammatory cytokine IL-1β and factor TNFα, as well as genes encoding NMDA- and kainate receptor subunits, which was established for the first time for this antioxidant enzyme. The protective effect of Prx-6 is due to its antioxidant properties, since mutant Prx-6 (mutPrx-6, Prx6-C47S) leads to polar opposite effects, contributing to oxidative stress, activation of apoptosis and cell death through receptor action on TLR4. Full article
(This article belongs to the Special Issue Role of Bioactive Molecules on Neuroprotection, Oxidative Stress and Neuroinflammation Modulation)
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Review

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20 pages, 919 KiB  
Review
Bidirectional Control between Cholesterol Shuttle and Purine Signal at the Central Nervous System
by Daniela Passarella, Maurizio Ronci, Valentina Di Liberto, Mariachiara Zuccarini, Giuseppa Mudò, Carola Porcile, Monica Frinchi, Patrizia Di Iorio, Henning Ulrich and Claudio Russo
Int. J. Mol. Sci. 2022, 23(15), 8683; https://doi.org/10.3390/ijms23158683 - 4 Aug 2022
Cited by 3 | Viewed by 2952
Abstract
Recent studies have highlighted the mechanisms controlling the formation of cerebral cholesterol, which is synthesized in situ primarily by astrocytes, where it is loaded onto apolipoproteins and delivered to neurons and oligodendrocytes through interactions with specific lipoprotein receptors. The “cholesterol shuttle” is influenced [...] Read more.
Recent studies have highlighted the mechanisms controlling the formation of cerebral cholesterol, which is synthesized in situ primarily by astrocytes, where it is loaded onto apolipoproteins and delivered to neurons and oligodendrocytes through interactions with specific lipoprotein receptors. The “cholesterol shuttle” is influenced by numerous proteins or carbohydrates, which mainly modulate the lipoprotein receptor activity, function and signaling. These molecules, provided with enzymatic/proteolytic activity leading to the formation of peptide fragments of different sizes and specific sequences, could be also responsible for machinery malfunctions, which are associated with neurological, neurodegenerative and neurodevelopmental disorders. In this context, we have pointed out that purines, ancestral molecules acting as signal molecules and neuromodulators at the central nervous system, can influence the homeostatic machinery of the cerebral cholesterol turnover and vice versa. Evidence gathered so far indicates that purine receptors, mainly the subtypes P2Y2, P2X7 and A2A, are involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer’s and Niemann–Pick C diseases, by controlling the brain cholesterol homeostasis; in addition, alterations in cholesterol turnover can hinder the purine receptor function. Although the precise mechanisms of these interactions are currently poorly understood, the results here collected on cholesterol–purine reciprocal control could hopefully promote further research. Full article
(This article belongs to the Special Issue Role of Bioactive Molecules on Neuroprotection, Oxidative Stress and Neuroinflammation Modulation)
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