Connection between Oxidative Stress and Hemorrhagic/Ischemic Cerebral Vascular Diseases

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 (30 September 2022) | Viewed by 21323

Special Issue Editors


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Guest Editor
Departments of Anesthesiology and Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA 92350, USA
Interests: cerebral vascular diseases; ischemic and hemorrhagic stroke; neuroprotective strategies; cerebral vascular biology; signaling pathways
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Department of Neurosurgery, Southwest Hospital, Army Medical University, Chongqing 400038, China
Interests: stroke; mitochondrial; cognitive dysfunction; neurons
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310027, China
Interests: stroke; intracerebral hemorrhage; subarachnoid hemorrhage; neuroinflammation; glioma

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Guest Editor
Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, FL 33612, USA
Interests: stroke; brain injury; neuroprotection; neuroscience; kinase; phosphorylation; cell biology

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Guest Editor
Department of Neurosurgery, Uludag University School of Medicine, Bursa 16059, Turkey
Interests: erebrovascular diseases; neurooncology; neuroprotective strategies; neuroscience; movement disorders; neuromodulation

Special Issue Information

Dear Colleagues,

Stroke can be classified into different types depending on the causes and clinical symptoms, including cerebral vascular blockage (ischemic stroke) or rupture (hemorrhagic stroke), and resulting in long-term neurological sequelae as well as great burdens to society. Inspired by the concept of the vascular neural network underlying both ischemic and hemorrhagic stroke, hypoxia due to disturbed intracranial circulation is considered to be the most common and key mechanism for secondary brain injury following stroke. Therefore, hypoxia-derived oxidative stress and neuroinflammation were widely reported to be potential therapeutic targets for acute cerebral vascular diseases. Among these complicated signaling networks, the multifunctional transcriptional factor Nrf2 was generally considered to play a core role and attracted the attention of neurologists for experimental and translational stroke studies.

In this Special Issue entitled “Connection between Oxidative Stress and Hemorrhagic/Ischemic Cerebral Vascular Disease”, we sincerely invite you to submit your latest research findings either as an original research or review article regarding the role of oxidative stress and neuroinflammation in cerebral vascular diseases. We encourage submissions on topics including but not limited to:

(1) Oxidative-stress-related pathophysiological mechanisms after stroke;
(2) Hypoxia-derived neuroinflammation and modulation strategies after stroke;
(3) Oxidative-stress-related subcellular organelle changes in neuronal and other cell types after stroke;
(4) Oxidative-stress-related programmed cell death in neuronal and other cell types after stroke;
(5) Cell–cell connections for maintaining neuronal functions under hypoxia and oxidative stress after stroke;
(6) Oxidative stress-related blood brain barrier disruption after stroke;
(7) Nrf2-related pharmacological targets and innovational compounds for the treatment of stroke.

Prof. Dr. John H. Zhang
Dr. Yujie Chen
Dr. Weilin Xu
Dr. Paul R. Krafft
Dr. Pınar Eser
Guest Editors

Manuscript Submission Information

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Keywords

  • hemorrhagic stroke
  • ischemic stroke
  • Nrf-2
  • oxidative stress
  • neuroinflammation
  • subcellular organelle
  • programmed cell death
  • blood brain barrier

Published Papers (5 papers)

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Research

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11 pages, 638 KiB  
Article
Association between Dietary Total Antioxidant Capacity of Antioxidant Vitamins and the Risk of Stroke among US Adults
by Chaojun Yang, Xiaocan Jia, Yuping Wang, Jingwen Fan, Chenyu Zhao, Yongli Yang and Xuezhong Shi
Antioxidants 2022, 11(11), 2252; https://doi.org/10.3390/antiox11112252 - 15 Nov 2022
Cited by 12 | Viewed by 1708
Abstract
The intake of antioxidant vitamins can scavenge free radicals and reduce oxidative stress, which may be beneficial for stroke. However, the relationship between total antioxidant capacity (TAC) of antioxidant vitamins and stroke is controversial. This study aims to investigate the association between dietary [...] Read more.
The intake of antioxidant vitamins can scavenge free radicals and reduce oxidative stress, which may be beneficial for stroke. However, the relationship between total antioxidant capacity (TAC) of antioxidant vitamins and stroke is controversial. This study aims to investigate the association between dietary TAC and the risk of stroke in US adults. This study included participants over 20 years old from the 2001–2018 National Health and Nutrition Examination Survey (NHANES). Data from two 24 h dietary recalls were used to estimate the usual intake of antioxidant vitamins. TAC was calculated by the vitamin C equivalent antioxidant capacity reference values of individual antioxidant vitamins. Survey-weighted generalized linear models were performed to evaluate the relationship between TAC and the risk of stroke. A restricted cubic spline regression model was used to investigate the dose–response association. A total of 37,045 participants was involved, of whom 1391 suffered a stroke. Compared with the first tertile, the participants in the second tertile of TAC showed a lower risk of stroke (OR = 0.788, 95% CI: 0.662, 0.936) after adjusting for potential risk factors. The dose–response analysis showed a gradual increase in the risk of stroke as TAC decreases. Subgroups analyses indicated that this association was primarily in the population of those aged over 60 years old, who were female, consumed alcohol, were a former smoker and inactive. The sensitivity analysis presented consistent results. These results suggest that deficiency of dietary TAC was associated with an increased risk of stroke, particularly in populations with underlying oxidative stress injury. Full article
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17 pages, 5667 KiB  
Article
Puerarin Attenuates Oxidative Stress and Ferroptosis via AMPK/PGC1α/Nrf2 Pathway after Subarachnoid Hemorrhage in Rats
by Yi Huang, Honggang Wu, Yongmei Hu, Chenhui Zhou, Jiawei Wu, Yiwen Wu, Haifeng Wang, Cameron Lenahan, Lei Huang, Sheng Nie, Xiang Gao and Jie Sun
Antioxidants 2022, 11(7), 1259; https://doi.org/10.3390/antiox11071259 - 27 Jun 2022
Cited by 47 | Viewed by 7944
Abstract
Puerarin was shown to exert anti-oxidative and anti-ferroptosis effects in multiple diseases. The goal of this study was to explore the neuroprotective effect of puerarin on early brain injury (EBI) after subarachnoid hemorrhage (SAH) in rats. A total of 177 adult male Sprague [...] Read more.
Puerarin was shown to exert anti-oxidative and anti-ferroptosis effects in multiple diseases. The goal of this study was to explore the neuroprotective effect of puerarin on early brain injury (EBI) after subarachnoid hemorrhage (SAH) in rats. A total of 177 adult male Sprague Dawley rats were used. SAH was included via endovascular perforation. Intranasal puerarin or intracerebroventricular dorsomorphin (AMPK inhibitor) and SR18292 (PGC1α inhibitor) were administered. The protein levels of pAMPK, PGC1α, Nrf2, 4HNE, HO1, MDA, ACSL4, GSSG, and iron concentration in the ipsilateral hemisphere were significantly increased, whereas SOD, GPX4, and GSH were decreased at 24 h after SAH. Moreover, puerarin treatment significantly increased the protein levels of pAMPK, PGC1α, Nrf2, HO1, SOD, GPX4, and GSH, but decreased the levels of 4HNE, MDA, ACSL4, GSSG, and iron concentration in the ipsilateral hemisphere at 24 h after SAH. Dorsomorphin or SR18292 partially abolished the beneficial effects of puerarin exerted on neurological dysfunction, oxidative stress injury, and ferroptosis. In conclusion, puerarin improved neurobehavioral impairments and attenuated oxidative-stress-induced brain ferroptosis after SAH in rats. The neuroprotection acted through the activation of the AMPK/PGC1α/Nrf2-signaling pathway. Thus, puerarin may serve as new therapeutics against EBI in SAH patients. Full article
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Review

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14 pages, 982 KiB  
Review
Oxidative Stress and Intracranial Hypertension after Aneurysmal Subarachnoid Hemorrhage
by Guangshan Hao, Pinar Eser and Jun Mo
Antioxidants 2022, 11(12), 2423; https://doi.org/10.3390/antiox11122423 - 8 Dec 2022
Cited by 5 | Viewed by 1406
Abstract
Intracranial hypertension is a common phenomenon in patients with aneurysmal subarachnoid hemorrhage (aSAH). Elevated intracranial pressure (ICP) plays an important role in early brain injuries and is associated with unfavorable outcomes. Despite advances in the management of aSAH, there is no consensus about [...] Read more.
Intracranial hypertension is a common phenomenon in patients with aneurysmal subarachnoid hemorrhage (aSAH). Elevated intracranial pressure (ICP) plays an important role in early brain injuries and is associated with unfavorable outcomes. Despite advances in the management of aSAH, there is no consensus about the mechanisms involved in ICP increases after aSAH. Recently, a growing body of evidence suggests that oxidative stress (OS) may play a crucial role in physio-pathological changes following aSAH, which may also contribute to increased ICP. Herein, we discuss a potential relation between increased ICP and OS, and resultantly propose antioxidant mechanisms as a potential therapeutic strategy for the treatment of ICP elevation following aSAH. Full article
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29 pages, 2787 KiB  
Review
Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke
by Lei Wang, Xu Zhang, Xiaoxing Xiong, Hua Zhu, Ran Chen, Shudi Zhang, Gang Chen and Zhihong Jian
Antioxidants 2022, 11(12), 2377; https://doi.org/10.3390/antiox11122377 - 30 Nov 2022
Cited by 60 | Viewed by 6125
Abstract
Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood [...] Read more.
Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood circulation will lead to cerebral ischemia-reperfusion injury (CIRI). Cerebral ischemic stroke involves many pathological processes such as oxidative stress, inflammation, and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2), as one of the most critical antioxidant transcription factors in cells, can coordinate various cytoprotective factors to inhibit oxidative stress. Targeting Nrf2 is considered as a potential strategy to prevent and treat cerebral ischemia injury. During cerebral ischemia, Nrf2 participates in signaling pathways such as Keap1, PI3K/AKT, MAPK, NF-κB, and HO-1, and then alleviates cerebral ischemia injury or CIRI by inhibiting oxidative stress, anti-inflammation, maintaining mitochondrial homeostasis, protecting the blood–brain barrier, and inhibiting ferroptosis. In this review, we have discussed the structure of Nrf2, the mechanisms of Nrf2 in cerebral ischemic stroke, the related research on the treatment of cerebral ischemia through the Nrf2 signaling pathway in recent years, and expounded the important role and future potential of the Nrf2 pathway in cerebral ischemic stroke. Full article
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27 pages, 1503 KiB  
Review
The Role of Concomitant Nrf2 Targeting and Stem Cell Therapy in Cerebrovascular Disease
by Jonah Gordon, Gavin Lockard, Molly Monsour, Adam Alayli and Cesario V. Borlongan
Antioxidants 2022, 11(8), 1447; https://doi.org/10.3390/antiox11081447 - 26 Jul 2022
Cited by 4 | Viewed by 2933
Abstract
Despite the reality that a death from cerebrovascular accident occurs every 3.5 min in the United States, there are few therapeutic options which are typically limited to a narrow window of opportunity in time for damage mitigation and recovery. Novel therapies have targeted [...] Read more.
Despite the reality that a death from cerebrovascular accident occurs every 3.5 min in the United States, there are few therapeutic options which are typically limited to a narrow window of opportunity in time for damage mitigation and recovery. Novel therapies have targeted pathological processes secondary to the initial insult, such as oxidative damage and peripheral inflammation. One of the greatest challenges to therapy is the frequently permanent damage within the CNS, attributed to a lack of sufficient neurogenesis. Thus, recent use of cell-based therapies for stroke have shown promising results. Unfortunately, stroke-induced inflammatory and oxidative damage limit the therapeutic potential of these stem cells. Nuclear factor erythroid 2-related factor 2 (Nrf2) has been implicated in endogenous antioxidant and anti-inflammatory activity, thus presenting an attractive target for novel therapeutics to enhance stem cell therapy and promote neurogenesis. This review assesses the current literature on the concomitant use of stem cell therapy and Nrf2 targeting via pharmaceutical and natural agents, highlighting the need to elucidate both upstream and downstream pathways in optimizing Nrf2 treatments in the setting of cerebrovascular disease. Full article
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