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Antioxidants
Special Issues
Oxidative Stress and Pathophysiology of Stroke
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Oxidative Stress and Pathophysiology of Stroke

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: 10 October 2024 | Viewed by 3067

Special Issue Editor

Dr. Klaus Van Leyen

E-Mail Website
Guest Editor
Neuroprotection Research Laboratories, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
Interests: stroke; brain injury; oxidative stress; neuroscience; neuropharmacology

Special Issue Information

Dear Colleagues,

In this Special Issue, we aim to provide both a broad overview of the role oxidative stress plays in causing brain injury following a stroke and of the varying approaches taken to treat strokes by reducing oxidative stress. Stroke is a devastating disease that represents one of the leading causes of death in the United States and worldwide. Treatment options using mechanical thrombectomy and improved brain imaging have enabled new ways of thinking about the sequence of events that is unleashed by the original ischemic event, which is typically when a blood clot blocks one of the major arteries of the brain. These treatments can now be used to target stroke injury mechanisms in ways that were not available just a few years ago. In parallel, it is now even more obvious how oxidative stress contributes to hemorrhagic forms of stroke, including both intracerebral and subarachnoid hemorrhage. It is necessary to gain an enhanced understanding of oxidative-stress-related mechanisms in all stroke subtypes to develop effective mechanism-based treatments that work.

We would like to receive a wide range of manuscripts highlighting both mechanistic studies to further elucidate the role of oxidative stress, as well as translational approaches that can lead to novel treatments. We anticipate a mixture of original studies and focused review articles that will provide a comprehensive snapshot of our current understanding of the role oxidative stress plays in the pathophysiology of stroke.

Dr. Klaus Van Leyen
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

  • ischemia
  • ischemia-reperfusion injury
  • lipoxygenase
  • glutathione peroxidase
  • superoxide dismutase
  • cyclooxygenase
  • ferroptosis
  • oxytosis
  • mitochondria
  • radical scavengers
  • antioxidants
  • redox enzymes
  • neurovascular injury
  • neuroprotection

Published Papers (3 papers)

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Research

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14 pages, 3838 KiB  
Article
Photobiomodulation Inhibits Ischemia-Induced Brain Endothelial Senescence via Endothelial Nitric Oxide Synthase
by Yu Feng, Zhihai Huang, Xiaohui Ma, Xuemei Zong, Vesna Tesic, Baojin Ding, Celeste Yin-Chieh Wu, Reggie Hui-Chao Lee and Quanguang Zhang
Antioxidants 2024, 13(6), 633; https://doi.org/10.3390/antiox13060633 - 23 May 2024
Viewed by 341
Abstract
Recent research suggests that photobiomodulation therapy (PBMT) positively impacts the vascular function associated with various cerebrovascular diseases. Nevertheless, the specific mechanisms by which PBMT improves vascular function remain ambiguous. Since endothelial nitric oxide synthase (eNOS) is crucial in regulating vascular function following cerebral [...] Read more.
Recent research suggests that photobiomodulation therapy (PBMT) positively impacts the vascular function associated with various cerebrovascular diseases. Nevertheless, the specific mechanisms by which PBMT improves vascular function remain ambiguous. Since endothelial nitric oxide synthase (eNOS) is crucial in regulating vascular function following cerebral ischemia, we investigated whether eNOS is a key element controlling cerebrovascular function and the senescence of vascular endothelial cells following PBMT treatment. Both rat photothrombotic (PT) stroke and in vitro oxygen–glucose deprivation (OGD)-induced vascular endothelial injury models were utilized. We demonstrated that treatment with PBMT (808 nm, 350 mW/cm2, 2 min/day) for 7 days significantly reduced PT-stroke-induced vascular permeability. Additionally, PBMT inhibited the levels of endothelial senescence markers (senescence green and p21) and antiangiogenic factor (endostatin), while increasing the phospho-eNOS (Ser1177) in the peri-infarct region following PT stroke. In vitro study further indicated that OGD increased p21, endostatin, and DNA damage (γH2AX) levels in the brain endothelial cell line, but they were reversed by PBMT. Intriguingly, the beneficial effects of PBMT were attenuated by a NOS inhibitor. In summary, these findings provide novel insights into the role of eNOS in PBMT-mediated protection against cerebrovascular senescence and endothelial dysfunction following ischemia. The use of PBMT as a therapeutic is a promising strategy to improve endothelial function in cerebrovascular disease. Full article
(This article belongs to the Special Issue Oxidative Stress and Pathophysiology of Stroke)
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20 pages, 1949 KiB  
Article
Long-Term Region-Specific Mitochondrial Functionality Changes in Both Cerebral Hemispheres after fMCAo Model of Ischemic Stroke
by Ksenija Lūcija Bahire, Reinis Maļuhins, Fiona Bello, Jolanta Upīte, Aleksandrs Makarovs and Baiba Jansone
Antioxidants 2024, 13(4), 416; https://doi.org/10.3390/antiox13040416 - 29 Mar 2024
Viewed by 700
Abstract
Cerebral ischemia/reperfusion (I/R) refers to a secondary brain injury that results in mitochondrial dysfunction of variable extent, leading to neuronal cell damage. The impact of this process has mainly been studied in the short term, from the early hours up to one week [...] Read more.
Cerebral ischemia/reperfusion (I/R) refers to a secondary brain injury that results in mitochondrial dysfunction of variable extent, leading to neuronal cell damage. The impact of this process has mainly been studied in the short term, from the early hours up to one week after blood flow reperfusion, and in the ischemic hemisphere only. The focus of this study was to assess the long-term impacts of I/R on mitochondrial functionality using high-resolution fluorespirometry to evaluate state-dependent activities in both ischemic (ipsilateral) and non-ischemic (contralateral) hemispheres of male mice 60, 90, 120, and 180 days after I/R caused by 60-min-long filament-induced middle cerebral artery occlusion (fMCAo). Our results indicate that in cortical tissues, succinate-supported oxygen flux (Complex I&II OXPHOS state) and H2O2 production (Complex II LEAK state) were significantly decreased in the fMCAo (stroke) group ipsilateral hemisphere compared to measurements in the contralateral hemisphere 60 and 90 days after stroke. In hippocampal tissues, during the Complex I&II ET state, mitochondrial respiration was generally lower in the ipsilateral compared to the contralateral hemisphere 90 days following stroke. An aging-dependent impact on mitochondria oxygen consumption following I/R injury was observed 180 days after surgery, wherein Complex I&II activities were lowest in both hemispheres. The obtained results highlight the importance of long-term studies in the field of ischemic stroke, particularly when evaluating mitochondrial bioenergetics in specific brain regions within and between separately affected cerebral hemispheres. Full article
(This article belongs to the Special Issue Oxidative Stress and Pathophysiology of Stroke)
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Review

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24 pages, 2958 KiB  
Review
Antioxidant and Anti-Inflammatory Effects of Garlic in Ischemic Stroke: Proposal of a New Mechanism of Protection through Regulation of Neuroplasticity
by Sandra Monserrat Bautista-Perez, Carlos Alfredo Silva-Islas, Oscar Uriel Sandoval-Marquez, Jesús Toledo-Toledo, José Manuel Bello-Martínez, Diana Barrera-Oviedo and Perla D. Maldonado
Antioxidants 2023, 12(12), 2126; https://doi.org/10.3390/antiox12122126 - 16 Dec 2023
Cited by 1 | Viewed by 1536
Abstract
Stroke represents one of the main causes of death and disability in the world; despite this, pharmacological therapies against stroke remain insufficient. Ischemic stroke is the leading etiology of stroke. Different molecular mechanisms, such as excitotoxicity, oxidative stress, and inflammation, participate in cell [...] Read more.
Stroke represents one of the main causes of death and disability in the world; despite this, pharmacological therapies against stroke remain insufficient. Ischemic stroke is the leading etiology of stroke. Different molecular mechanisms, such as excitotoxicity, oxidative stress, and inflammation, participate in cell death and tissue damage. At a preclinical level, different garlic compounds have been evaluated against these mechanisms. Additionally, there is evidence supporting the participation of garlic compounds in other mechanisms that contribute to brain tissue recovery, such as neuroplasticity. After ischemia, neuroplasticity is activated to recover cognitive and motor function. Some garlic-derived compounds and preparations have shown the ability to promote neuroplasticity under physiological conditions and, more importantly, in cerebral damage models. This work describes damage/repair mechanisms and the importance of garlic as a source of antioxidant and anti-inflammatory agents against damage. Moreover, we examine the less-explored neurotrophic properties of garlic, culminating in proposals and observations based on our review of the available information. The aim of the present study is to propose that garlic compounds and preparations could contribute to the treatment of ischemic stroke through their neurotrophic effects. Full article
(This article belongs to the Special Issue Oxidative Stress and Pathophysiology of Stroke)
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