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Natural Products and Neuroprotection 3.0
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Natural Products and Neuroprotection 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 50110

Special Issue Editors

Dr. Cristina Angeloni

E-Mail Website
Guest Editor
Department for Life Quality Studies, Alma Mater Studiorum-University of Bologna, Corso D’Augusto 237, 47921 Rimini, Italy
Interests: nutritional biochemistry; neurodegenerative diseases; oxidative stress; inflammation; nutraceuticals; ageing
Special Issues, Collections and Topics in MDPI journals
Dr. David Vauzour

E-Mail Website
Guest Editor
Norwich Medical School, Faculty of Medicine and Health Sciences, University of East Anglia, Norwich NR4 7UQ, UK
Interests: neurodegenerative disorders; phytochemicals; neuroinflammation; memory; learning and neuro-cognitive performances; signalling pathways; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are among the most serious health problems affecting millions of people worldwide, and their incidence is dramatically growing together with increased lifespan. These diseases are a heterogenous group of chronic, progressive disorders characterized by the gradual loss of neurons in the central nervous system, which leads to deficits in specific brain functions. The most common neurodegenerative diseases are Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, and Huntington’s disease. These multifactorial debilitating disorders share common molecular and cellular characteristics, such as oxidative stress, mitochondrial dysfunction, protein misfolding, excitotoxicity, and inflammation. Presently, there are no therapeutic approaches to cure or even halt the progression of these disorders. In this context, natural products, because of their broad spectrum of pharmacological and biological activities, are considered promising alternatives for the treatment of neurodegeneration. Natural compounds have been recognized to possess different biological activities, including antioxidant, anti-inflammatory, and antiapoptotic effects. Moreover, natural compounds have been recently shown to counteract protein misfolding and to modulate autophagy and proteasome activity.

In this Special Issue, we invite investigators to contribute original research articles, as well as review articles regarding the biological effect of natural products in preventing/counteracting neurodegeneration.

Topics include but are not limited to the following:

  • Clinical or preclinical studies investigating natural products in the treatment of neurodegenerative diseases;
  • The role of natural products in counteracting oxidative stress in neurodegeneration;
  • The role of natural products in counteracting inflammation in neurodegeneration;
  • The use of natural products in modulating autophagy and proteasome activity to counteract abnormal protein aggregation in neurodegeneration;
  • The role of natural products in modulating signalling pathways involved in neurodegeneration;
  • The use of natural products as lead compounds in drug discovery for the treatment of neurodegenerative diseases.

Prof. Cristina Angeloni
Prof. Dr. David Vauzour
Guest Editors

Manuscript Submission Information

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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

  • oxidative stress
  • inflammation
  • protein misfolding
  • natural compounds
  • nutraceuticals
  • phytochemicals
  • neurodegeneration
  • alzheimer’s disease
  • parkinson’s disease
  • amyotrophic lateral sclerosis
  • multiple sclerosis
  • huntington’s disease

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Published Papers (12 papers)

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Editorial

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4 pages, 190 KiB  
Editorial
Natural Products and Neuroprotection 3.0
by Cristina Angeloni and David Vauzour
Int. J. Mol. Sci. 2023, 24(4), 3885; https://doi.org/10.3390/ijms24043885 - 15 Feb 2023
Cited by 2 | Viewed by 1455
Abstract
In recent years, we have been witnessing a dramatic rise in the incidence of neurodegenerative diseases, a phenomenon partly associated with the increase in life expectancy [...] Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)

Research

Jump to: Editorial, Review, Other

20 pages, 3591 KiB  
Article
Anti-Inflammatory Effect of Beta-Caryophyllene Mediated by the Involvement of TRPV1, BDNF and trkB in the Rat Cerebral Cortex after Hypoperfusion/Reperfusion
by Maria Pina Serra, Marianna Boi, Antonella Carta, Elisabetta Murru, Gianfranca Carta, Sebastiano Banni and Marina Quartu
Int. J. Mol. Sci. 2022, 23(7), 3633; https://doi.org/10.3390/ijms23073633 - 26 Mar 2022
Cited by 10 | Viewed by 3191
Abstract
We have previously shown that bilateral common carotid artery occlusion followed by reperfusion (BCCAO/R) is a model to study early hypoperfusion/reperfusion-induced changes in biomarkers of the tissue physiological response to oxidative stress and inflammation. Thus in this study, we investigate with immunochemical assays [...] Read more.
We have previously shown that bilateral common carotid artery occlusion followed by reperfusion (BCCAO/R) is a model to study early hypoperfusion/reperfusion-induced changes in biomarkers of the tissue physiological response to oxidative stress and inflammation. Thus in this study, we investigate with immunochemical assays if a single dose of beta-caryophyllene (BCP), administered before the BCCAO/R, can modulate the TRPV1, BDNF, and trkB receptor in the brain cortex; the glial markers GFAP and Iba1 were also examined. Frontal and temporal-occipital cortical regions were analyzed in two groups of male rats, sham-operated and submitted to BCCAO/R. Six hours before surgery, one group was gavage fed a dose of BCP (40 mg/per rat in 300 μL of sunflower oil), the other was pre-treated with the vehicle alone. Western blot analysis showed that, in the frontal cortex of vehicle-treated rats, the BCCAO/R caused a TRPV1 decrease, an increment of trkB and GFAP, no change in BDNF and Iba1. The BCP treatment caused a decrease of BDNF and an increase of trkB levels in both sham and BCCAO/R conditions while inducing opposite changes in the case of TRPV1, whose levels became higher in BCCAO/R and lower in sham conditions. Present results highlight the role of BCP in modulating early events of the cerebral inflammation triggered by the BCCAO/R through the regulation of TRPV1 and the BDNF-trkB system. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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14 pages, 5185 KiB  
Article
Deciphering the Potential Neuroprotective Effects of Luteolin against Aβ1–42-Induced Alzheimer’s Disease
by Sareer Ahmad, Myeung Hoon Jo, Muhammad Ikram, Amjad Khan and Myeong Ok Kim
Int. J. Mol. Sci. 2021, 22(17), 9583; https://doi.org/10.3390/ijms22179583 - 3 Sep 2021
Cited by 60 | Viewed by 5350
Abstract
The current study was undertaken to unveil the protective effects of Luteolin, a natural flavonoid, against amyloid-beta (Aβ1–42)-induced neuroinflammation, amyloidogenesis, and synaptic dysfunction in mice. For the development of an AD mouse model, amyloid-beta (Aβ1–42, [...] Read more.
The current study was undertaken to unveil the protective effects of Luteolin, a natural flavonoid, against amyloid-beta (Aβ1–42)-induced neuroinflammation, amyloidogenesis, and synaptic dysfunction in mice. For the development of an AD mouse model, amyloid-beta (Aβ1–42, 5 μL/5 min/mouse) oligomers were injected intracerebroventricularly (i.c.v.) into mice’s brain by using a stereotaxic frame. After that, the mice were treated with Luteolin for two weeks at a dose of 80 mg/kg/day. To monitor the biochemical changes, we conducted western blotting and immunofluorescence analysis. According to our findings, the infusion of amyloid-beta activated c-Jun N-terminal kinases (p-JNK), p38 mitogen-activated protein kinases, glial fibrillary acidic protein (GFAP), and ionized calcium adaptor molecule 1 (Iba-1) in the cortex and hippocampus of the experimental mice; these changes were significantly inhibited in Aβ1–42 + Luteolin-treated mice. Likewise, we also checked the expression of inflammatory markers, such as p-nuclear factor-kB p65 (p-NF-kB p65 (Ser536), tissue necrosis factor (TNF-α), and Interleukin1-β (IL-1β), in Aβ1–42-injected mice brain, which was attenuated in Aβ1–42 + Luteolin-treated mice brains. Further, we investigated the expression of pro- and anti-apoptotic cell death markers such as Bax, Bcl-2, Caspase-3, and Cox-2, which was significantly reduced in Aβ1–42 + Lut-treated mice brains compared to the brains of the Aβ-injected group. The results also indicated that with the administration of Aβ1–42, the expression levels of β-site amyloid precursor protein cleaving enzyme (BACE-1) and amyloid-beta (Aβ1–42) were significantly enhanced, while they were reduced in Aβ1–42 + Luteolin-treated mice. We also checked the expression of synaptic markers such as PSD-95 and SNAP-25, which was significantly enhanced in Aβ1–42 + Lut-treated mice. To unveil the underlying factors responsible for the protective effects of Luteolin against AD, we used a specific JNK inhibitor, which suggested that Luteolin reduced Aβ-associated neuroinflammation and neurodegeneration via inhibition of JNK. Collectively, our results indicate that Luteolin could serve as a novel therapeutic agent against AD-like pathological changes in mice. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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15 pages, 2872 KiB  
Communication
Neuroprotection Mediated by Human Blood Plasma in Mouse Hippocampal Slice Cultures and in Oxidatively Stressed Human Neurons
by Lucia M. Ruiz-Perera, Anna L. Höving, Kazuko E. Schmidt, Sule Cenan, Max Wohllebe, Johannes F. W. Greiner, Christian Kaltschmidt, Matthias Simon, Cornelius Knabbe and Barbara Kaltschmidt
Int. J. Mol. Sci. 2021, 22(17), 9567; https://doi.org/10.3390/ijms22179567 - 3 Sep 2021
Cited by 5 | Viewed by 2716
Abstract
Neuroprotection from oxidative stress is critical during neuronal development and maintenance but also plays a major role in the pathogenesis and potential treatment of various neurological disorders and neurodegenerative diseases. Emerging evidence in the murine system suggests neuroprotective effects of blood plasma on [...] Read more.
Neuroprotection from oxidative stress is critical during neuronal development and maintenance but also plays a major role in the pathogenesis and potential treatment of various neurological disorders and neurodegenerative diseases. Emerging evidence in the murine system suggests neuroprotective effects of blood plasma on the aged or diseased brain. However, little is known about plasma-mediated effects on human neurons. In the present study, we demonstrate the neuroprotective effect mediated by human plasma and the most abundant plasma–protein human serum albumin against oxidative stress in glutamatergic neurons differentiated from human neural crest-derived inferior turbinate stem cells. We observed a strong neuroprotective effect of human plasma and human serum albumin against oxidative stress-induced neuronal death on the single cell level, similar to the one mediated by tumor necrosis factor alpha. Moreover, we detected neuroprotection of plasma and human serum albumin against kainic acid-induced excitatory stress in ex vivo cultured mouse hippocampal tissue slices. The present study provides deeper insights into plasma-mediated neuroprotection ultimately resulting in the development of novel therapies for a variety of neurological and, in particular, neurodegenerative diseases. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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19 pages, 18705 KiB  
Article
Effects of Urolithin A on Mitochondrial Parameters in a Cellular Model of Early Alzheimer Disease
by Carsten Esselun, Ellen Theyssen and Gunter P. Eckert
Int. J. Mol. Sci. 2021, 22(15), 8333; https://doi.org/10.3390/ijms22158333 - 3 Aug 2021
Cited by 32 | Viewed by 6274
Abstract
(1) Background: Ellagitannins are natural products occurring in pomegranate and walnuts. They are hydrolyzed in the gut to release ellagic acid, which is further metabolized by the microflora into urolithins, such as urolithin A (UA). Accumulation of damaged mitochondria is a hallmark of [...] Read more.
(1) Background: Ellagitannins are natural products occurring in pomegranate and walnuts. They are hydrolyzed in the gut to release ellagic acid, which is further metabolized by the microflora into urolithins, such as urolithin A (UA). Accumulation of damaged mitochondria is a hallmark of aging and age-related neurodegenerative diseases. In this study, we investigated the neuroprotective activity of the metabolite UA against mitochondrial dysfunction in a cellular model of early Alzheimer disease (AD). (2) Methods: In the present study we used SH-SY5Y-APP695 cells and its corresponding controls (SH-SY5Ymock) to assess UA’s effect on mitochondrial function. Using these cells we investigated mitochondrial respiration (OXPHOS), mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) production, autophagy and levels of reactive oxygen species (ROS) in cells treated with UA. Furthermore, we assessed UA’s effect on the expression of genes related to mitochondrial bioenergetics, mitochondrial biogenesis, and autophagy via quantitative real-time PCR (qRT-PCR). (3) Results: Treatment of SH-SY5Y-APP695 cells suggests changes to autophagy corresponding with qRT-PCR results. However, LC3B-I, LC3B-II, and p62 levels were unchanged. UA (10 µM) reduced MMP, and ATP-levels. Treatment of cells with UA (1 µM) for 24 h did not affect ROS production or levels of Aβ, but significantly increased expression of genes for mitochondrial biogenesis and OXPHOS. Mitochondrial Transcription Factor A (TFAM) expression was specifically increased in SH-SY5Y-APP695. Both cell lines showed unaltered levels of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), which is commonly associated with mitochondrial biogenesis. Results imply that biogenesis might be facilitated by estrogen-related receptor (ESRR) genes. (4) Conclusion: Urolithin A shows no effect on autophagy in SH-SY5Y-APP695 cells and its effect on mitochondrial function is limited. Instead, data suggests that UA treatment induces hormetic effects as it induces transcription of several genes related to mitochondrial biogenesis. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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17 pages, 1376 KiB  
Article
Curcumin Potentiates α7 Nicotinic Acetylcholine Receptors and Alleviates Autistic-Like Social Deficits and Brain Oxidative Stress Status in Mice
by Petrilla Jayaprakash, Dmytro Isaev, Waheed Shabbir, Dietrich E. Lorke, Bassem Sadek and Murat Oz
Int. J. Mol. Sci. 2021, 22(14), 7251; https://doi.org/10.3390/ijms22147251 - 6 Jul 2021
Cited by 20 | Viewed by 4646
Abstract
Autistic spectrum disorder (ASD) refers to a group of neurodevelopmental disorders characterized by impaired social interaction and cognitive deficit, restricted repetitive behaviors, altered immune responses, and imbalanced oxidative stress status. In recent years, there has been a growing interest in studying the role [...] Read more.
Autistic spectrum disorder (ASD) refers to a group of neurodevelopmental disorders characterized by impaired social interaction and cognitive deficit, restricted repetitive behaviors, altered immune responses, and imbalanced oxidative stress status. In recent years, there has been a growing interest in studying the role of nicotinic acetylcholine receptors (nAChRs), specifically α7-nAChRs, in the CNS. Influence of agonists for α7-nAChRs on the cognitive behavior, learning, and memory formation has been demonstrated in neuro-pathological condition such as ASD and attention-deficit hyperactivity disorder (ADHD). Curcumin (CUR), the active compound of the spice turmeric, has been shown to act as a positive allosteric modulator of α7-nAChRs. Here we hypothesize that CUR, acting through α7-nAChRs, influences the neuropathology of ASD. In patch clamp studies, fast inward currents activated by choline, a selective agonist of α7-nAChRs, were significantly potentiated by CUR. Moreover, choline induced enhancement of spontaneous inhibitory postsynaptic currents was markedly increased in the presence of CUR. Furthermore, CUR (25, 50, and 100 mg/kg, i.p.) ameliorated dose-dependent social deficits without affecting locomotor activity or anxiety-like behaviors of tested male Black and Tan BRachyury (BTBR) mice. In addition, CUR (50 and 100 mg/kg, i.p.) mitigated oxidative stress status by restoring the decreased levels of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus and the cerebellum of treated mice. Collectively, the observed results indicate that CUR potentiates α7-nAChRs in native central nervous system neurons, mitigates disturbed oxidative stress, and alleviates ASD-like features in BTBR mice used as an idiopathic rodent model of ASD, and may represent a promising novel pharmacological strategy for ASD treatment. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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22 pages, 7348 KiB  
Article
RETRACTED: Thymoquinone and Curcumin Defeat Aging-Associated Oxidative Alterations Induced by D-Galactose in Rats’ Brain and Heart
by Ali H. El-Far, Yaser H. A. Elewa, Elsayeda-Zeinab A. Abdelfattah, Abdel-Wahab A. Alsenosy, Mustafa S. Atta, Khalid M. Abou-Zeid, Soad K. Al Jaouni, Shaker A. Mousa and Ahmed E. Noreldin
Int. J. Mol. Sci. 2021, 22(13), 6839; https://doi.org/10.3390/ijms22136839 - 25 Jun 2021
Cited by 17 | Viewed by 4223 | Retraction
Abstract
D-galactose (D-gal) administration causes oxidative disorder and is widely utilized in aging animal models. Therefore, we subcutaneously injected D-gal at 200 mg/kg BW dose to assess the potential preventive effect of thymoquinone (TQ) and curcumin (Cur) against the oxidative alterations induced by D-gal. [...] Read more.
D-galactose (D-gal) administration causes oxidative disorder and is widely utilized in aging animal models. Therefore, we subcutaneously injected D-gal at 200 mg/kg BW dose to assess the potential preventive effect of thymoquinone (TQ) and curcumin (Cur) against the oxidative alterations induced by D-gal. Other than the control, vehicle, and D-gal groups, the TQ and Cur treated groups were orally supplemented at 20 mg/kg BW of each alone or combined. TQ and Cur effectively suppressed the oxidative alterations induced by D-gal in brain and heart tissues. The TQ and Cur combination significantly decreased the elevated necrosis in the brain and heart by D-gal. It significantly reduced brain caspase 3, calbindin, and calcium-binding adapter molecule 1 (IBA1), heart caspase 3, and BCL2. Expression of mRNA of the brain and heart TP53, p21, Bax, and CASP-3 were significantly downregulated in the TQ and Cur combination group along with upregulation of BCL2 in comparison with the D-gal group. Data suggested that the TQ and Cur combination is a promising approach in aging prevention. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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33 pages, 15042 KiB  
Article
Neuroprotective Metabolites of Hericium erinaceus Promote Neuro-Healthy Aging
by Elisa Roda, Erica Cecilia Priori, Daniela Ratto, Fabrizio De Luca, Carmine Di Iorio, Paola Angelone, Carlo Alessandro Locatelli, Anthea Desiderio, Lorenzo Goppa, Elena Savino, Maria Grazia Bottone and Paola Rossi
Int. J. Mol. Sci. 2021, 22(12), 6379; https://doi.org/10.3390/ijms22126379 - 15 Jun 2021
Cited by 40 | Viewed by 7879
Abstract
Frailty is a geriatric syndrome associated with both locomotor and cognitive decline, typically linked to chronic systemic inflammation, i.e., inflammaging. In the current study, we investigated the effect of a two-month oral supplementation with standardized extracts of H. erinaceus, containing a [...] Read more.
Frailty is a geriatric syndrome associated with both locomotor and cognitive decline, typically linked to chronic systemic inflammation, i.e., inflammaging. In the current study, we investigated the effect of a two-month oral supplementation with standardized extracts of H. erinaceus, containing a known amount of Erinacine A, Hericenone C, Hericenone D, and L-ergothioneine, on locomotor frailty and cerebellum of aged mice. Locomotor performances were monitored comparing healthy aging and frail mice. Cerebellar volume and cytoarchitecture, together with inflammatory and oxidative stress pathways, were assessed focusing on senescent frail animals. H. erinaceus partially recovered the aged-related decline of locomotor performances. Histopathological analyses paralleled by immunocytochemical evaluation of specific molecules strengthened the neuroprotective role of H. erinaceus able to ameliorate cerebellar alterations, i.e., milder volume reduction, slighter molecular layer thickness decrease and minor percentage of shrunken Purkinje neurons, also diminishing inflammation and oxidative stress in frail mice while increasing a key longevity regulator and a neuroprotective molecule. Thus, our present findings demonstrated the efficacy of a non-pharmacological approach, based on the dietary supplementation using H. erinaceus extract, which represent a promising adjuvant therapy to be associated with conventional geriatric treatments. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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16 pages, 3816 KiB  
Article
Effect of Berberine Isolated from Barberry Species by Centrifugal Partition Chromatography on Memory and the Expression of Parvalbumin in the Mouse Hippocampus Proper
by Radosław Szalak, Wirginia Kukula-Koch, Małgorzata Matysek, Marta Kruk-Słomka, Wojciech Koch, Lidia Czernicka, Daariimaa Khurelbat, Grażyna Biała and Marcin B. Arciszewski
Int. J. Mol. Sci. 2021, 22(9), 4487; https://doi.org/10.3390/ijms22094487 - 26 Apr 2021
Cited by 9 | Viewed by 2643
Abstract
Neurodegenerative diseases associated with memory disturbances are important health issues occurring due to a prolonged life span. This article presents the results of a study targeting the emergence of a drug candidate with antiamnesic properties. The effect of berberine (BBR), an isoquinoline alkaloid [...] Read more.
Neurodegenerative diseases associated with memory disturbances are important health issues occurring due to a prolonged life span. This article presents the results of a study targeting the emergence of a drug candidate with antiamnesic properties. The effect of berberine (BBR), an isoquinoline alkaloid isolated from the overground parts of Berberis sibirica Pall., on memory and expression of parvalbumin in the mouse hippocampus proper were determined. High-purity BBR was isolated by centrifugal partition chromatography from a methanolic extract from B. sibirica by using a methyl-tert-butyl ether and water (1:1 v/v) solvent system with 10 mmol/L of triethylamine and hydrochloric acid. In an in vivo study, we assessed the influence of the chronic administration of BBR on different stages of memory-related responses in mice. Our results indicated that the chronic administration of BBR in a higher dose (5 mg/kg) improves long-term memory acquisition in mice, as determined in the passive avoidance test. The hippocampal CA1–CA3 fields showed an increased number of parvalbumin-immunoreactive neurons (PV-IR) and nerve fibers as compared to the control. No significant changes in the dentate gyrus were observed between the groups. The HPLC-ESI-QTOF-MS/MS analysis of the biological material revealed the content of BBR as 363.4 ± 15.0 ng (4.11% of RSD) per brain, 15.06 ± 0.89 ng (5.91% of RSD) per hippocampus, and 54.45 ± 1.40 (4.05% of RSD) ng in 100 µL plasma. The study showed that BBR could be a factor influencing the expression of PV in hippocampal neurons. We speculate that BBR may modulate the level of Ca2+ in neurons and thus potentially act as a neuroprotective factor against neuronal damages. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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18 pages, 12212 KiB  
Article
Quercetin Attenuates Brain Oxidative Alterations Induced by Iron Oxide Nanoparticles in Rats
by Mohamed F. Dora, Nabil M. Taha, Mohamed A. Lebda, Aml E. Hashem, Mohamed S. Elfeky, Yasser S. El-Sayed, Soad Al Jaouni and Ali H. El-Far
Int. J. Mol. Sci. 2021, 22(8), 3829; https://doi.org/10.3390/ijms22083829 - 7 Apr 2021
Cited by 28 | Viewed by 3488
Abstract
Iron oxide nanoparticle (IONP) therapy has diverse health benefits but high doses or prolonged therapy might induce oxidative cellular injuries especially in the brain. Therefore, we conducted the current study to investigate the protective role of quercetin supplementation against the oxidative alterations induced [...] Read more.
Iron oxide nanoparticle (IONP) therapy has diverse health benefits but high doses or prolonged therapy might induce oxidative cellular injuries especially in the brain. Therefore, we conducted the current study to investigate the protective role of quercetin supplementation against the oxidative alterations induced in the brains of rats due to IONPs. Forty adult male albino rats were allocated into equal five groups; the control received a normal basal diet, the IONP group was intraperitoneally injected with IONPs of 50 mg/kg body weight (B.W.) and quercetin-treated groups had IONPs + Q25, IONPs + Q50 and IONPs + Q100 that were orally supplanted with quercetin by doses of 25, 50 and 100 mg quercetin/kg B.W. daily, respectively, administrated with the same dose of IONPs for 30 days. IONPs induced significant increases in malondialdehyde (MDA) and significantly decreased reduced glutathione (GSH) and oxidized glutathione (GSSG). Consequently, IONPs significantly induced severe brain tissue injuries due to the iron deposition leading to oxidative alterations with significant increases in brain creatine phosphokinase (CPK) and acetylcholinesterase (AChE). Furthermore, IONPs induced significant reductions in brain epinephrine, serotonin and melatonin with the downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and mitochondrial transcription factor A (mtTFA) mRNA expressions. IONPs induced apoptosis in the brain monitored by increases in caspase 3 and decreases in B-cell lymphoma 2 (Bcl2) expression levels. Quercetin supplementation notably defeated brain oxidative damages and in a dose-dependent manner. Therefore, quercetin supplementation during IONPs is highly recommended to gain the benefits of IONPs with fewer health hazards. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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Review

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21 pages, 935 KiB  
Review
Can Natural Products Exert Neuroprotection without Crossing the Blood–Brain Barrier?
by Manon Leclerc, Stéphanie Dudonné and Frédéric Calon
Int. J. Mol. Sci. 2021, 22(7), 3356; https://doi.org/10.3390/ijms22073356 - 25 Mar 2021
Cited by 27 | Viewed by 6064
Abstract
The scope of evidence on the neuroprotective impact of natural products has been greatly extended in recent years. However, a key question that remains to be answered is whether natural products act directly on targets located in the central nervous system (CNS), or [...] Read more.
The scope of evidence on the neuroprotective impact of natural products has been greatly extended in recent years. However, a key question that remains to be answered is whether natural products act directly on targets located in the central nervous system (CNS), or whether they act indirectly through other mechanisms in the periphery. While molecules utilized for brain diseases are typically bestowed with a capacity to cross the blood–brain barrier, it has been recently uncovered that peripheral metabolism impacts brain functions, including cognition. The gut–microbiota–brain axis is receiving increasing attention as another indirect pathway for orally administered compounds to act on the CNS. In this review, we will briefly explore these possibilities focusing on two classes of natural products: omega-3 polyunsaturated fatty acids (n-3 PUFAs) from marine sources and polyphenols from plants. The former will be used as an example of a natural product with relatively high brain bioavailability but with tightly regulated transport and metabolism, and the latter as an example of natural compounds with low brain bioavailability, yet with a growing amount of preclinical and clinical evidence of efficacy. In conclusion, it is proposed that bioavailability data should be sought early in the development of natural products to help identifying relevant mechanisms and potential impact on prevalent CNS disorders, such as Alzheimer’s disease. Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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Other

1 pages, 153 KiB  
Retraction
RETRACTED: El-Far et al. Thymoquinone and Curcumin Defeat Aging-Associated Oxidative Alterations Induced by D-Galactose in Rats’ Brain and Heart. Int. J. Mol. Sci. 2021, 22, 6839
by Ali H. El-Far, Yaser H. A. Elewa, Elsayeda-Zeinab A. Abdelfattah, Abdel-Wahab A. Alsenosy, Mustafa S. Atta, Khalid M. Abou-Zeid, Soad K. Al Jaouni, Shaker A. Mousa and Ahmed E. Noreldin
Int. J. Mol. Sci. 2024, 25(23), 13063; https://doi.org/10.3390/ijms252313063 - 5 Dec 2024
Viewed by 376
Abstract
The International Journal of Molecular Sciences retracts the article “Thymoquinone and Curcumin Defeat Aging-Associated Oxidative Alterations Induced by D-Galactose in Rats’ Brain and Heart” [...] Full article
(This article belongs to the Special Issue Natural Products and Neuroprotection 3.0)
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