ArticleScientific reports2016
Methazolamide improves neurological behavior by inhibition of neuron apoptosis in subarachnoid hemorrhage mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Mechanisms of memory impairment in animal models of nontraumatic intracranial hemorrhage: A systematic review of the literature.Brain hemorrhages · 2022Pooled it
- Alzheimer's Disease Pathogenic Mechanisms: Linking Redox Homeostasis and Mitochondria-Associated Metabolic Pathways Through Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2).Antioxidants (Basel, Switzerland) · 2025Review
- The MT1 receptor as the target of ramelteon neuroprotection in ischemic stroke.Journal of pineal research · 2024Article
- The mechanism and relevant mediators associated with neuronal apoptosis and potential therapeutic targets in subarachnoid hemorrhage.Neural regeneration research · 2023Review
- Brain edema formation and therapy after intracerebral hemorrhage.Neurobiology of disease · 2023Review
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Andrographolide Attenuates Blood-Brain Barrier Disruption, Neuronal Apoptosis, and Oxidative Stress Through Activation of Nrf2/HO-1 Signaling Pathway in Subarachnoid Hemorrhage.Neurotoxicity research · 2022Article
- ACE2 Rescues Impaired Autophagic Flux Through the PI3K/AKT Pathway After Subarachnoid Hemorrhage.Neurochemical research · 2022Article
- Carbonic Anhydrases as Potential Targets Against Neurovascular Unit Dysfunction in Alzheimer's Disease and Stroke.Frontiers in aging neuroscience · 2021Review
- Nrf2 activation through the PI3K/GSK-3 axis protects neuronal cells from Aβ-mediated oxidative and metabolic damage.Alzheimer's research & therapy · 2020Article
- Tartary buckwheat extract alleviates alcohol-induced acute and chronic liver injuries through the inhibition of oxidative stress and mitochondrial cell death pathway.American journal of translational research · 2020Article
- Morphological Characteristics of Neuronal Death After Experimental Subarachnoid Hemorrhage in Mice Using Double Immunoenzymatic Technique.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Article
- Tetramethylpyrazine Nitrone Reduces Oxidative Stress to Alleviate Cerebral Vasospasm in Experimental Subarachnoid Hemorrhage Models.Neuromolecular medicine · 2019Article
- The effect of intravascular interventional embolization and craniotomy on MMP-2, MMP-9 and caspase3 in serum of intracranial aneurysm patients.Experimental and therapeutic medicine · 2018Article
- Cerebral influx of NaFluids and barriers of the CNS · 2018Article
- Cerebroprotection by salvianolic acid B after experimental subarachnoid hemorrhage occurs via Nrf2- and SIRT1-dependent pathways.Free radical biology & medicine · 2018Article
- Mitochondrial Dysfunction in Stroke: Implications of Stem Cell Therapy.Translational stroke research · 2018Review
- The Role of Smurf1 in Neuronal Necroptosis after Lipopolysaccharide-Induced Neuroinflammation.Cellular and molecular neurobiology · 2018Article
- P450 Eicosanoids and Reactive Oxygen Species Interplay in Brain Injury and Neuroprotection.Antioxidants & redox signaling · 2018Article
- P2X7 Receptor-Associated Programmed Cell Death in the Pathophysiology of Hemorrhagic Stroke.Current neuropharmacology · 2018Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subarachnoid hemorrhage (SAH) results in significant nerve dysfunction, such as hemiplegia, mood disorders, cognitive and memory impairment. Currently, no clear measures can reduce brain nerve damage. The study of brain nerve protection after SAH is of great significance. We aim to evaluate the protective effects and the possible mechanism of methazolamide in C57BL/6J SAH animal model in vivo and in blood-induced primary cortical neuron (PCNs) cellular model of SAH in vitro. We demonstrate that methazolamide accelerates the recovery of neurological damage, effectively relieves cerebral edema, and improves cognitive function in SAH mice as well as offers neuroprotection in blood- or hemoglobin-treated PCNs and partially restores normal neuronal morphology. In addition, western blot analyses show obviously decreased expression of active caspase-3 in methazolamide-treated SAH mice comparing with vehicle-treated SAH animals. Furthermore, methazolamide effectively inhibits ROS production in PCNs induced by blood exposure or hemoglobin insult. However, methazolamide has no protective effects in morality, fluctuation of cerebral blood flow, SAH grade, and cerebral vasospasm of SAH mice. Given methazolamide, a potent carbonic anhydrase inhibitor, can penetrate the blood-brain barrier and has been used in clinic in the treatment of ocular conditions, it provides potential as a novel therapy for SAH.
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