ArticleExperimental neurology2015
Reduction of zinc accumulation in mitochondria contributes to decreased cerebral ischemic injury by normobaric hyperoxia treatment in an experimental stroke model.
Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Multimodal Neuroprotection in Ischemic Stroke: Emerging Non-Pharmacological Interventions from Bench to Bedside.Brain sciences · 2025Review
- Synthesis of Fluorescent Pyrazoline Sensors as Versatile Tool for Zinc ion Detection: A Mini-Review.Journal of fluorescence · 2025Review
- Normobaric Hyperoxia Therapy in Treating Stroke.Clinical interventions in aging · 2025Review
- The neuroprotective effects of normobaric oxygen therapy after stroke.CNS neuroscience & therapeutics · 2024Review
- Normobaric hyperoxia alleviates complement C3-mediated synaptic pruning and brain injury after intracerebral hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Review
- Zinc accumulation aggravates cerebral ischemia/reperfusion injury by promoting inflammation.Frontiers in cellular neuroscience · 2023Article
- The Important Role of Zinc in Neurological Diseases.Biomolecules · 2022Review
- Zinc improves neurological recovery by promoting angiogenesis via the astrocyte-mediated HIF-1α/VEGF signaling pathway in experimental stroke.CNS neuroscience & therapeutics · 2022Article
- Increased Mobile Zinc Regulates Retinal Ganglion Cell Survival via Activating Mitochondrial OMA1 and Integrated Stress Response.Antioxidants (Basel, Switzerland) · 2022Article
- Normobaric hyperoxia plays a neuroprotective role after cerebral ischemia by maintaining the redox homeostasis and the level of connexin43 in astrocytes.CNS neuroscience & therapeutics · 2022Article
- Zinc Accumulation Aggravates Cerebral Ischemia/Reperfusion Injury Through Inducing Endoplasmic Reticulum Stress.Neurochemical research · 2022Article
- IKKα contributes to ischemia-induced autophagy after acute cerebral ischemic injury.Annals of translational medicine · 2022Article
- Endogenous zinc protoporphyrin formation critically contributes to hemorrhagic stroke-induced brain damage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Article
- Zinc cytotoxicity induces mitochondrial morphology changes in hela cell line.International journal of physiology, pathophysiology and pharmacology · 2021Article
- Normobaric Oxygen May Ameliorate Cerebral Venous Outflow Disturbance-Related Neurological Symptoms.Frontiers in neurology · 2020Article
- Normobaric oxygen: a novel approach for treating chronic cerebral circulation insufficiency.Clinical interventions in aging · 2019Article
- Synergistic Interaction Between Zinc and Reactive Oxygen Species Amplifies Ischemic Brain Injury in Rats.Stroke · 2018Article
- Pathophysiological role of zinc in ischemic brain injury.Oncotarget · 2017Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Cerebral ischemia interrupts oxygen supply to the affected tissues. Our previous studies have reported that normobaric hyperoxia (NBO) can maintain interstitial partial pressure of oxygen (pO2) in the penumbra of ischemic stroke rats at the physiological level, thus affording significant neuroprotection. However, the mechanisms that are responsible for the penumbra rescue by NBO treatment are not fully understood. Recent studies have shown that zinc, an important mediator of intracellular and intercellular neuronal signaling, accumulates in neurons and leads to ischemic neuronal injury. In this study, we investigate whether NBO could regulate zinc accumulation in the penumbra and prevent mitochondrial damage in penumbral tissue using a transient cerebral ischemic rat model. Our results showed that NBO significantly reduced zinc-staining positive cells and zinc-staining intensity in penumbral tissues, but not in the ischemic core. Moreover, ischemia-induced zinc accumulation in mitochondria, isolated from penumbral tissues, was greatly attenuated by NBO or a zinc-specific chelator, N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN). NBO or TPEN administration stabilized the mitochondrial membrane potential in the penumbra after cerebral ischemia. Finally, ischemia-induced cytochrome c release from mitochondria in penumbral tissues was significantly reduced by NBO or TPEN treatment. These findings demonstrate a novel mechanism for NBO's neuroprotection, especially to penumbral tissues, providing further evidence for the potential clinical benefit of NBO for acute ischemic stroke.
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