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Polyphenolic Compounds as Neuroprotective Agents

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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 July 2019) | Viewed by 22123

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Special Issue Editor

Prof. Dr. Daniel Linseman

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Guest Editor

Department of Biological Sciences, Knoebel Institute for Healthy Aging, University of Denver, Denver, CO 80208, USA
Interests: nutraceuticals; antioxidants; neuronal apoptosis; neurodegeneration; neurotrauma; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative and nitrosative stress are characterized by the aberrant production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively. The deleterious effects of ROS and RNS are characterized by enhanced lipid peroxidation, oxidative damage to proteins and DNA, and mitochondrial dysfunction, often leading to cell death via apoptosis or necrosis. These processes are hallmarks of neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, as well as brain ischemia and neurotrauma. Antioxidants exhibit intrinsic free radical scavenging activity, making them potential therapeutic agents for these disorders. Polyphenols are natural bioactive compounds that are under active investigation for their antioxidant, anti-nitrosative, and anti-inflammatory properties. Many polyphenolic compounds have also been shown to influence endogenous antioxidant systems via the Nrf2/Keap1 pathway. In addition, polyphenolic compounds modulate the balance of pro-apoptotic and anti-apoptotic proteins, such as those of the Bcl-2 family. All of these mechanisms likely contribute to the neuroprotective properties of this family of natural compounds. Polyphenols are divided into several classes according to their chemical structures, including flavonoids, phenolic acids, tannins, stilbenes, and lignans. Their structures contain one or more phenolic units, which contributes to their intrinsic free radical scavenging activity via the donation of hydrogen and stable resonance structures of the rings. Exploiting the antioxidant, anti-nitrosative, and anti-inflammatory properties of naturally occurring polyphenolic compounds, as well as their effects on Nrf2/Keap1 and apoptotic signaling pathways, has the potential to identify novel therapeutic agents for neurodegenerative diseases and episodes of ischemia and neurotrauma. This Special Issue of Antioxidants invites submissions of both reviews of the literature as well as original research articles describing the neuroprotective effects of polyphenolic compounds in cell culture systems, preclinical animal models, and human clinical studies.

Prof. Dr. Daniel Linseman
Guest Editor

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Keywords

polyphenols
nutraceuticals
antioxidants
neuroprotection
neurodegeneration
apoptosis
Nrf2/Keap1

Published Papers (3 papers)

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Research

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20 pages, 6629 KiB

Open AccessArticle

Anti-Oxidant Activity of Gallotannin-Enriched Extract of Galla Rhois Can Associate with the Protection of the Cognitive Impairment through the Regulation of BDNF Signaling Pathway and Neuronal Cell Function in the Scopolamine-Treated ICR Mice

by Ji Won Park, Ji Eun Kim, Mi Ju Kang, Hyeon Jun Choi, Su Ji Bae, Sou Hyun Kim, Young Suk Jung, Jin Tae Hong and Dae Youn Hwang

Antioxidants 2019, 8(10), 450; https://doi.org/10.3390/antiox8100450 - 3 Oct 2019

Cited by 13 | Viewed by 5853

Abstract

The antibacterial, anti-inflammatory, anti-metastatic/anti-invasion activities and laxative activity of Galla Rhois (GR) are well-known, although the neuropreservation effects of their extracts are still to be elucidated. To investigate the novel therapeutic effects and molecular mechanism of GR on alleviation of cognitive impairment, two different dosages of gallotannin-enriched GR (GEGR) were administered to Korl:ICR mice for three weeks, and to induce memory impairment, scopolamine (SP) was administered during the last seven days of the GEGR treatment period. GEGR showed the high level of the free radical scavenging activity to DPPH and suppressive activity to reactive oxygen species (ROS) in B35 cells as well as enhanced SOD and CAT activity in brains of the SP-induced model. Latency time for memory impairment assessed by the passive avoidance test significantly protected in the SP+GEGR treated group as compared to the SP+Vehicle treated group. Moreover, similar protective effects were observed on the secretion of BDNF in SP+GEGR treated mice. The expression of TrkB receptor, and phosphorylation of PI3K on the TrkB receptor signaling pathway were dramatically protected in the SP-induced model after GEGR treatment, whereas the expression of p75^NTR receptor, the phosphorylation of JNK, and expression of Bax/Bcl-2 on the p75^NTR receptor signaling pathway was significantly protected in the same group. Furthermore, the GEGR treated SP-induced model showed decreased number of dead neural cells and suppressed acetylcholine esterase (AChE) activity and inhibited inflammatory responses. Taken together, these results indicate that the anti-oxidant activity of GEGR contributes to improving the neuronal cell function and survival during cognitive impairment in the SP-induced model through regulation of BDNF secretion and their receptor signaling pathway. Full article

(This article belongs to the Special Issue Polyphenolic Compounds as Neuroprotective Agents)

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19 pages, 1778 KiB

Open AccessCommunication

Timing of Treatment with the Flavonoid 7,8-DHF Critically Impacts on Its Effects on Learning and Memory in the Ts65Dn Mouse

by Andrea Giacomini, Fiorenza Stagni, Marco Emili, Beatrice Uguagliati, Roberto Rimondini, Renata Bartesaghi and Sandra Guidi

Antioxidants 2019, 8(6), 163; https://doi.org/10.3390/antiox8060163 - 6 Jun 2019

Cited by 15 | Viewed by 3816

Abstract

No therapies currently exist for intellectual disability in Down syndrome (DS). In view of its similarities with DS, including learning and memory (L&M) defects, the Ts65Dn mouse model of DS is widely used for the design of therapy. 7,8-dihydroxyflavone (7,8-DHF), a flavonoid that targets the tropomyosin-related kinase B (TrkB) receptor of brain-derived neurotrophic factor (BDNF), exerts positive effects in various brain disease models. Based on previous demonstration that administration of 7,8-DHF in the postnatal period P3-P15 restores hippocampal neurogenesis and spinogenesis, we sought to establish whether these effects translate into behavioral benefits after treatment cessation. We found that Ts65Dn mice treated with 7,8-DHF (5.0 mg/kg/day) during postnatal days P3-P15 did not show any L&M improvement at one month after treatment cessation, indicating that the effects of 7,8-DHF on the brain are ephemeral. Based on evidence that chronic treatment with 7,8-DHF in juvenile Ts65Dn mice restores L&M, we sought to establish whether a similar effect is elicited in adulthood. We found that Ts65Dn mice treated with 7,8-DHF (5.0 mg/kg/day) for about 40 days starting from 4 months of age did not show any improvement in L&M. The results suggest that timing of therapy with 7,8-DHF is a critical issue for attainment of positive effects on the brain. Full article

(This article belongs to the Special Issue Polyphenolic Compounds as Neuroprotective Agents)

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Review

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45 pages, 3781 KiB

Open AccessReview

Anthocyanins and Their Metabolites as Therapeutic Agents for Neurodegenerative Disease

by Aimee N. Winter and Paula C. Bickford

Antioxidants 2019, 8(9), 333; https://doi.org/10.3390/antiox8090333 - 22 Aug 2019

Cited by 100 | Viewed by 12100

Abstract

Neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS), are characterized by the death of neurons within specific regions of the brain or spinal cord. While the etiology of many neurodegenerative diseases remains elusive, several factors are thought to contribute to the neurodegenerative process, such as oxidative and nitrosative stress, excitotoxicity, endoplasmic reticulum stress, protein aggregation, and neuroinflammation. These processes culminate in the death of vulnerable neuronal populations, which manifests symptomatically as cognitive and/or motor impairments. Until recently, most treatments for these disorders have targeted single aspects of disease pathology; however, this strategy has proved largely ineffective, and focus has now turned towards therapeutics which target multiple aspects underlying neurodegeneration. Anthocyanins are unique flavonoid compounds that have been shown to modulate several of the factors contributing to neuronal death, and interest in their use as therapeutics for neurodegeneration has grown in recent years. Additionally, due to observations that the bioavailability of anthocyanins is low relative to that of their metabolites, it has been proposed that anthocyanin metabolites may play a significant part in mediating the beneficial effects of an anthocyanin-rich diet. Thus, in this review, we will explore the evidence evaluating the neuroprotective and therapeutic potential of anthocyanins and their common metabolites for treating neurodegenerative diseases. Full article

(This article belongs to the Special Issue Polyphenolic Compounds as Neuroprotective Agents)

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