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Antioxidants
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The Role of Natural Antioxidants in Neuroinflammation
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The Role of Natural Antioxidants in Neuroinflammation

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 (20 October 2022) | Viewed by 20008

Special Issue Editor

Prof. Dr. Teresa Trotta

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy
Interests: inflammation; cytokines; microglia; cell signalling; apoptosis; polyphenols; natural compounds; antioxidants

Special Issue Information

Dear Colleagues,

Neuroinflammation is a defence mechanism aimed to protect the nervous system in response to a variety of insults. It is characterized by the activation of microglia and astrocyte population and production of pro-inflammatory molecules and, if perpetuated, inflammation becomes chronic with prolonged and intensified expression of pro-inflammatory cytokines and reactive oxygen species, causing severe damage to the neuronal compartment.

In the last decade, neuroinflammation has taken on an increasingly important role in the pathogenesis and progression of many neurodegenerative and neurological disorders such as Parkinson's disease, Alzheimer’s disease, Multiple Sclerosis, Huntington's disease, as well as those that develop after traumatic injury.

Due to a lack of clinically efficacious drugs, the use of natural antioxidants may provide an alternative therapy that prevents oxidative stress and reduces neurological disease progression.

In this Special Issue titled "The Role of Natural Antioxidants in Neuroinflammation," we invite researchers to provide original research articles and review articles in the field of neuroinflammation, taking into account the role and mechanism of action of natural antioxidants.

Prof. Dr. Teresa Trotta
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

  • Neuroinflammation
  • Neuroprotection
  • Degenerative diseases
  • Microglia
  • Cytokines
  • Reactive oxygen species
  • Antioxidants
  • Natural compounds

Published Papers (7 papers)

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Research

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18 pages, 3539 KiB  
Article
Maternal Supplementation with N-Acetylcysteine Modulates the Microbiota-Gut-Brain Axis in Offspring of the Poly I:C Rat Model of Schizophrenia
by Diego Romero-Miguel, Marta Casquero-Veiga, Javier Fernández, Nicolás Lamanna-Rama, Vanessa Gómez-Rangel, Carlos Gálvez-Robleño, Cristina Santa-Marta, Claudio J. Villar, Felipe Lombó, Raquel Abalo, Manuel Desco and María Luisa Soto-Montenegro
Antioxidants 2023, 12(4), 970; https://doi.org/10.3390/antiox12040970 - 20 Apr 2023
Cited by 1 | Viewed by 1966
Abstract
The microbiota-gut-brain axis is a complex interconnected system altered in schizophrenia. The antioxidant N-acetylcysteine (NAC) has been proposed as an adjunctive therapy to antipsychotics in clinical trials, but its role in the microbiota-gut-brain axis has not been sufficiently explored. We aimed to describe [...] Read more.
The microbiota-gut-brain axis is a complex interconnected system altered in schizophrenia. The antioxidant N-acetylcysteine (NAC) has been proposed as an adjunctive therapy to antipsychotics in clinical trials, but its role in the microbiota-gut-brain axis has not been sufficiently explored. We aimed to describe the effect of NAC administration during pregnancy on the gut-brain axis in the offspring from the maternal immune stimulation (MIS) animal model of schizophrenia. Pregnant Wistar rats were treated with PolyI:C/Saline. Six groups of animals were studied according to the study factors: phenotype (Saline, MIS) and treatment (no NAC, NAC 7 days, NAC 21 days). Offspring were subjected to the novel object recognition test and were scanned using MRI. Caecum contents were used for metagenomics 16S rRNA sequencing. NAC treatment prevented hippocampal volume reduction and long-term memory deficits in MIS-offspring. In addition, MIS-animals showed lower bacterial richness, which was prevented by NAC. Moreover, NAC7/NAC21 treatments resulted in a reduction of proinflammatory taxons in MIS-animals and an increase in taxa known to produce anti-inflammatory metabolites. Early approaches, like this one, with anti-inflammatory/anti-oxidative compounds, especially in neurodevelopmental disorders with an inflammatory/oxidative basis, may be useful in modulating bacterial microbiota, hippocampal size, as well as hippocampal-based memory impairments. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidants in Neuroinflammation)
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13 pages, 2686 KiB  
Article
Yomogin, Isolated from Artemisia iwayomogi, Inhibits Neuroinflammation Stimulated by Lipopolysaccharide via Regulating MAPK Pathway
by Jin Hee Kim, In Gyoung Ju, Namkwon Kim, Eugene Huh, So-Ri Son, Joon Pyo Hong, Yujin Choi, Dae Sik Jang and Myung Sook Oh
Antioxidants 2023, 12(1), 106; https://doi.org/10.3390/antiox12010106 - 31 Dec 2022
Cited by 3 | Viewed by 2278
Abstract
Neuroinflammation causes various neurological disorders, including depression and neurodegenerative diseases. Therefore, regulation of neuroinflammation is a promising therapeutic strategy for inflammation-related neurological disorders. This study aimed to investigate whether yomogin, isolated from Artemisia iwayomogi, has anti-neuroinflammatory effects. First, we evaluated the effects of [...] Read more.
Neuroinflammation causes various neurological disorders, including depression and neurodegenerative diseases. Therefore, regulation of neuroinflammation is a promising therapeutic strategy for inflammation-related neurological disorders. This study aimed to investigate whether yomogin, isolated from Artemisia iwayomogi, has anti-neuroinflammatory effects. First, we evaluated the effects of yomogin by assessing pro-inflammatory mediators and cytokines in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. The results showed that yomogin inhibited the increase in neuroinflammatory factors, including nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-α, and suppressed phosphorylation of c-Jun N-terminal kinase, extracellular signal-regulated kinase and p38, which participate in the mitogen-activated protein kinase (MAPK) pathway. To confirm these effects in vivo, we measured the activation of astrocyte and microglia in LPS-injected mouse brains. Results showed that yomogin treatment decreased astrocyte and microglia activations. Collectively, these results suggest that yomogin suppresses neuroinflammation by regulating the MAPK pathway and it could be a potential candidate for inflammation-mediated neurological diseases. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidants in Neuroinflammation)
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16 pages, 1681 KiB  
Article
Comparable Benefits of Stingless Bee Honey and Caffeic Acid in Mitigating the Negative Effects of Metabolic Syndrome on the Brain
by Nellysha Namela Muhammad Abdul Kadar, Fairus Ahmad, Seong Lin Teoh and Mohamad Fairuz Yahaya
Antioxidants 2022, 11(11), 2154; https://doi.org/10.3390/antiox11112154 - 31 Oct 2022
Cited by 6 | Viewed by 2170
Abstract
There is mounting evidence that metabolic syndrome (MetS) contributes to the development of neurodegenerative disorders such as Alzheimer’s disease. Honey, which has been used for generations, is high in antioxidants and has been demonstrated to benefit the brain and mental health by reducing [...] Read more.
There is mounting evidence that metabolic syndrome (MetS) contributes to the development of neurodegenerative disorders such as Alzheimer’s disease. Honey, which has been used for generations, is high in antioxidants and has been demonstrated to benefit the brain and mental health by reducing oxidative stress and boosting cognitive outcomes. Honey from the stingless bees of Heterotrigona itama has been found to have higher phenolic content compared to other types of honeys. The aim of this study is to investigate the effects of stingless bee honey (SBH) supplementation and to compare it with a pure form of antioxidant, caffeic acid (CA), on MetS parameters and inflammatory markers in the brains of MetS-induced rats. A total of 32 male Wistar rats were divided equally into groups of control, high-carbohydrate high-fructose (HCHF) diet (MetS), HCHF + SBH supplemented (1 g/kg) (SBH), and HCHF + CA supplemented (10 mg/kg) (CA) groups. The total duration for SBH and CA supplementation was eight weeks. The HCHF diet was found to promote hypertension, hyperglycemia, and hypertriglyceridemia, and to increase brain TNF-α levels. Supplementation with SBH and CA significantly reversed (p < 0.05) the hyperglycemic and hypertensive effects of the HCHF diet. Although both supplemented groups showed no significant changes to serum HDL or TG, SBH significantly reduced (p < 0.05) brain TNF-α levels and increased (p < 0.05) brain BDNF levels. Immunohistochemistry investigations of neurogenesis (EdU) and apoptosis (TUNEL) on the cornu Ammonis 1 (CA1) and dentate gyrus (DG) areas of the hippocampus showed no changes with SBH and CA supplementation compared to the control. These findings suggest that SBH and CA have the potential to mitigate HCHF-induced MetS effects and possess neuroprotective abilities. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidants in Neuroinflammation)
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21 pages, 3823 KiB  
Article
2,3,5,4′-Tetrahydroxystilbene-2-O-β-glucoside Attenuates Reactive Oxygen Species-Dependent Inflammation and Apoptosis in Porphyromonas gingivalis-Infected Brain Endothelial Cells
by Vichuda Charoensaensuk, Yen-Chou Chen, Yun-Ho Lin, Keng-Liang Ou, Liang-Yo Yang and Dah-Yuu Lu
Antioxidants 2022, 11(4), 740; https://doi.org/10.3390/antiox11040740 - 08 Apr 2022
Viewed by 1973
Abstract
We recently reported that the periodontopathic bacteria Porphyromonas gingivalis (P. gingivalis) initiates an inflammatory cascade that disrupts the balance of reactive oxygen species (ROS), resulting in apoptotic cell death in brain endothelial cells. An extract from Polygonum multiflorum Thunb., 2,3,5,4′-Tetrahydroxystilbene-2-O-β-glucoside (THSG) [...] Read more.
We recently reported that the periodontopathic bacteria Porphyromonas gingivalis (P. gingivalis) initiates an inflammatory cascade that disrupts the balance of reactive oxygen species (ROS), resulting in apoptotic cell death in brain endothelial cells. An extract from Polygonum multiflorum Thunb., 2,3,5,4′-Tetrahydroxystilbene-2-O-β-glucoside (THSG) has been well-reported to diminish the inflammation in many disease models. However, the effects of THSG in the area of the brain–oral axis is unknown. In this study, we examined the effects of THSG in P. gingivalis-stimulated inflammatory response and apoptotic cell death in brain endothelial cells. THSG treatment remarkably lessened the upregulation of IL-1β and TNF-α proteins in bEnd.3 cells infected with P. gingivalis. Treatment of THSG further ameliorated brain endothelial cell death, including apoptosis caused by P. gingivalis. Moreover, the present study showed that the inhibitory effects on NF-κB p65 and antiapoptotic properties of THSG is through inhibiting the ROS pathway. Importantly, the ROS inhibitory potency of THSG is similar to a ROS scavenger N-Acetyl-L-Cysteine (NAC) and NADPH oxidase inhibitor apocynin. Furthermore, the protective effect of THSG from P. gingivalis infection was further confirmed in primary mouse brain endothelial cells. Taken together, this study indicates that THSG attenuates an ROS-dependent inflammatory response and cell apoptosis in P. gingivalis-infected brain endothelial cells. Our results also suggest that THSG could be a potential herbal medicine to prevent the risk of developing cerebrovascular diseases from infection of periodontal bacteria. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidants in Neuroinflammation)
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24 pages, 6905 KiB  
Article
Powdered Green Tea (Matcha) Attenuates the Cognitive Dysfunction via the Regulation of Systemic Inflammation in Chronic PM2.5-Exposed BALB/c Mice
by Jong Min Kim, Jin Yong Kang, Seon Kyeong Park, Jong Hyun Moon, Min Ji Kim, Hyo Lim Lee, Hye Rin Jeong, Jong Cheol Kim and Ho Jin Heo
Antioxidants 2021, 10(12), 1932; https://doi.org/10.3390/antiox10121932 - 30 Nov 2021
Cited by 14 | Viewed by 3035
Abstract
This study was conducted to evaluate the anti-amnesic effect of the aqueous extract of powdered green tea (matcha) (EM) in particulate matter (PM)2.5-induced systemic inflammation in BALB/c mice. EM ameliorated spatial learning and memory function, short-term memory function, and long-term learning [...] Read more.
This study was conducted to evaluate the anti-amnesic effect of the aqueous extract of powdered green tea (matcha) (EM) in particulate matter (PM)2.5-induced systemic inflammation in BALB/c mice. EM ameliorated spatial learning and memory function, short-term memory function, and long-term learning and memory function in PM2.5-induced mice. EM protected against antioxidant deficit in pulmonary, dermal, and cerebral tissues. In addition, EM improved the cholinergic system through the regulation of acetylcholine (ACh) levels and acetylcholinesterase (AChE) activity in brain tissue, and it protected mitochondrial dysfunction by regulating the production of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and ATP contents in brain tissue. EM attenuated systemic inflammation and apoptotic signaling in pulmonary, dermal, olfactory bulb, and hippocampal tissues. Moreover, EM suppressed neuronal cytotoxicity and cholinergic dysfunction in hippocampal tissue. This study suggests that EM might be a potential substance to improve PM2.5-induced cognitive dysfunction via the regulation of systemic inflammation. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidants in Neuroinflammation)
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19 pages, 40144 KiB  
Article
17β-Estradiol Abrogates Oxidative Stress and Neuroinflammation after Cortical Stab Wound Injury
by Kamran Saeed, Myeung Hoon Jo, Jun Sung Park, Sayed Ibrar Alam, Ibrahim Khan, Riaz Ahmad, Amjad Khan, Rahat Ullah and Myeong Ok Kim
Antioxidants 2021, 10(11), 1682; https://doi.org/10.3390/antiox10111682 - 25 Oct 2021
Cited by 13 | Viewed by 2382
Abstract
Disruptions in brain energy metabolism, oxidative damage, and neuroinflammation are commonly seen in traumatic brain injury (TBI). Microglial activation is the hallmark of neuroinflammation. After brain injury, microglia also act as a double-edged sword with distinctive phenotypic changes. Therefore, therapeutic applications to potentiate [...] Read more.
Disruptions in brain energy metabolism, oxidative damage, and neuroinflammation are commonly seen in traumatic brain injury (TBI). Microglial activation is the hallmark of neuroinflammation. After brain injury, microglia also act as a double-edged sword with distinctive phenotypic changes. Therefore, therapeutic applications to potentiate microglia towards pro-inflammatory response following brain injury have become the focus of attention in recent years. Here, in the current study, we investigated the hypothesis that 17β-estradiol could rescue the mouse brain against apoptotic cell death and neurodegeneration by suppressing deleterious proinflammatory response probably by abrogating metabolic stress and oxidative damage after brain injury. Male C57BL/6N mice were used to establish a cortical stab wound injury (SWI) model. Immediately after brain injury, the mice were treated with 17β-estradiol (10 mg/kg, once every day via i.p. injection) for one week. Immunoblotting and immunohistochemical analysis was performed to examine the cortical and hippocampal brain regions. For the evaluation of reactive oxygen species (ROS), reduced glutathione (GSH), and oxidized glutathione (GSSG), we used specific kits. Our findings revealed that 17β-estradiol treatment significantly alleviated SWI-induced energy dyshomeostasis and oxidative stress by increasing the activity of phospho-AMPK (Thr172) and by regulating the expression of an antioxidant gene (Nrf2) and cytoprotective enzymes (HO-1 and GSH) to mitigate ROS. Importantly, 17β-estradiol treatment downregulated gliosis and proinflammatory markers (iNOS and CD64) while significantly augmenting an anti-inflammatory response as evidenced by the robust expression of TGF-β and IGF-1 after brain injury. The treatment with 17β-estradiol also reduced inflammatory mediators (Tnf-α, IL-1β, and COX-2) in the injured mouse. Moreover, 17β-estradiol administration rescued p53-associated apoptotic cell death in the SWI model by regulating the expression of Bcl-2 family proteins (Bax and Bcl-2) and caspase-3 activation. Finally, SWI + 17β-estradiol-treated mice illustrated reduced brain lesion volume and enhanced neurotrophic effect and the expression of synaptic proteins. These findings suggest that 17β-estradiol is an effective therapy against the brain secondary injury-induced pathological cascade following trauma, although further studies may be conducted to explore the exact mechanisms. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidants in Neuroinflammation)
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Review

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24 pages, 1079 KiB  
Review
Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative
by Cindy Bandala, Noemi Cárdenas-Rodríguez, Samuel Reyes-Long, José Luis Cortes-Altamirano, David Garciadiego-Cázares, Eleazar Lara-Padilla, Gabriela Ibáñez-Cervantes, Javier Mancilla-Ramírez, Saul Gómez-Manzo and Alfonso Alfaro-Rodríguez
Antioxidants 2022, 11(10), 1972; https://doi.org/10.3390/antiox11101972 - 01 Oct 2022
Cited by 3 | Viewed by 4799
Abstract
Obesity remains a global health problem. Chronic low-grade inflammation in this pathology has been related to comorbidities such as cognitive alterations that, in the long term, can lead to neurodegenerative diseases. Neuroinflammation or gliosis in patients with obesity and type 2 diabetes mellitus [...] Read more.
Obesity remains a global health problem. Chronic low-grade inflammation in this pathology has been related to comorbidities such as cognitive alterations that, in the long term, can lead to neurodegenerative diseases. Neuroinflammation or gliosis in patients with obesity and type 2 diabetes mellitus has been related to the effect of adipokines, high lipid levels and glucose, which increase the production of free radicals. Cerebral gliosis can be a risk factor for developing neurodegenerative diseases, and antioxidants could be an alternative for the prevention and treatment of neural comorbidities in obese patients. Aim: Identify the immunological and oxidative stress mechanisms that produce gliosis in patients with obesity and propose antioxidants as an alternative to reducing neuroinflammation. Method: Advanced searches were performed in scientific databases: PubMed, ProQuest, EBSCO, and the Science Citation index for research on the physiopathology of gliosis in obese patients and for the possible role of antioxidants in its management. Conclusion: Patients with obesity can develop neuroinflammation, conditioned by various adipokines, excess lipids and glucose, which results in an increase in free radicals that must be neutralized with antioxidants to reduce gliosis and the risk of long-term neurodegeneration. Full article
(This article belongs to the Special Issue The Role of Natural Antioxidants in Neuroinflammation)
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