ArticleScientific reports2020
Characterization of a novel model of global forebrain ischaemia-reperfusion injury in mice and comparison with focal ischaemic and haemorrhagic stroke.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- The active role of pulmonary immunity in ischaemic stroke.Journal of neuroinflammation · 2026Review
- Gamma-Benzylidene Digoxin Derivative Attenuates Neurotoxicity Response in a Murine Stroke Model.Translational stroke research · 2025Article
- Ivermectin's neuroprotective effects decrease with prolonged use after cerebral ischemia/reperfusion.Metabolic brain disease · 2025Article
- Endothelial -targeted CD39 is protective in a mouse model of global forebrain ischaemia.Journal of neuroinflammation · 2025Article
- Efficacy of Omega-5 NanoPSO Treatment in the Hippocampus, Through Antioxidant Mechanisms, After an Ischemia/Reperfusion Injury, in Murine Model.Antioxidants (Basel, Switzerland) · 2024Article
- Targeting lipid nanoparticles to the blood-brain barrier to ameliorate acute ischemic stroke.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Global Cerebral Ischemia-induced Depression Accompanies Alteration of Neuronal Excitability in the Infralimbic Cortex Layer 2/3 Pyramidal Neurons.Experimental neurobiology · 2023Article
- The Effect of Cerebrolysin in an Animal Model of Forebrain Ischemic-Reperfusion Injury: New Insights into the Activation of the Keap1/Nrf2/Antioxidant Signaling Pathway.International journal of molecular sciences · 2023Article
- Article
- N-Terminomic Changes in Neurons During Excitotoxicity Reveal Proteolytic Events Associated With Synaptic Dysfunctions and Potential Targets for Neuroprotection.Molecular & cellular proteomics : MCP · 2023Article
- The Duration of Oxygen and Glucose Deprivation (OGD) Determines the Effects of Subsequent Reperfusion on Rat Pheochromocytoma (PC12) Cells and Primary Cortical Neurons.International journal of molecular sciences · 2023Article
- Targeted drug delivery to the brain endothelium dominates over passive delivery via vascular leak in experimental intracerebral hemorrhage.Journal of controlled release : official journal of the Controlled Release Society · 2023Article
- Tilapia Skin Peptides Ameliorate Cyclophosphamide-Induced Anxiety- and Depression-Like BehaviorFrontiers in nutrition · 2022Article
- Early Endothelial Activation in a Mouse Model of Graft vs Host Disease Following Chemotherapy.Frontiers in immunology · 2021Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke is caused by obstructed blood flow (ischaemia) or unrestricted bleeding in the brain (haemorrhage). Global brain ischaemia occurs after restricted cerebral blood flow e.g. during cardiac arrest. Following ischaemic injury, restoration of blood flow causes ischaemia-reperfusion (I/R) injury which worsens outcome. Secondary injury mechanisms after any stroke are similar, and encompass inflammation, endothelial dysfunction, blood-brain barrier (BBB) damage and apoptosis. We developed a new model of transient global forebrain I/R injury (dual carotid artery ligation; DCAL) and compared the manifestations of this injury with those in a conventional I/R injury model (middle-cerebral artery occlusion; MCAo) and with intracerebral haemorrhage (ICH; collagenase model). MRI revealed that DCAL produced smaller bilateral lesions predominantly localised to the striatum, whereas MCAo produced larger focal corticostriatal lesions. After global forebrain ischaemia mice had worse overall neurological scores, although quantitative locomotor assessment showed MCAo and ICH had significantly worsened mobility. BBB breakdown was highest in the DCAL model while apoptotic activity was highest after ICH. VCAM-1 upregulation was specific to ischaemic models only. Differential transcriptional upregulation of pro-inflammatory chemokines and cytokines and TLRs was seen in the three models. Our findings offer a unique insight into the similarities and differences in how biological processes are regulated after different types of stroke. They also establish a platform for analysis of therapies such as endothelial protective and anti-inflammatory agents that can be applied to all types of stroke.
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