ArticleStroke2012
CHOP silencing reduces acute brain injury in the rat model of subarachnoid hemorrhage.
Article in Stroke, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 71 citations in OpenAlex.
- IFP35, a novel DAMP, aggravates neuroinflammation following acute ischemic stroke via TLR4/NF-κB/NLRP3 signaling.Journal of neuroinflammation · 2025Article
- Paederoside, an active metabolite of Paederia scandens, alleviates osteoporosis by modulating Wnt/β-catenin signaling.Frontiers in pharmacology · 2025Article
- How to Use the Cuprizone Model to Study De- and Remyelination.International journal of molecular sciences · 2024Review
- Early Brain Injury and Neuroprotective Treatment after Aneurysmal Subarachnoid Hemorrhage: A Literature Review.Brain sciences · 2023Review
- Bim Deletion Reduces Functional Deficits Following Ischemic Stroke in Association with Modulation of Apoptosis and Inflammation.Neuromolecular medicine · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Ferritinophagy is Involved in Experimental Subarachnoid Hemorrhage-Induced Neuronal Ferroptosis.Neurochemical research · 2022Article
- Melatonin as a Potential Neuroprotectant: Mechanisms in Subarachnoid Hemorrhage-Induced Early Brain Injury.Frontiers in aging neuroscience · 2022Review
- Article
- Hepcidin Promoted Ferroptosis through Iron Metabolism which Is Associated with DMT1 Signaling Activation in Early Brain Injury following Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2021Article
- NLRP6 contributes to inflammation and brain injury following intracerebral haemorrhage by activating autophagy.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Review
- Ambroxol Improves Neuronal Survival and Reduces White Matter Damage through Suppressing Endoplasmic Reticulum Stress in Microglia after Intracerebral Hemorrhage.BioMed research international · 2020Article
- Article
- Thioredoxin-interacting protein mediates mitochondrion-dependent apoptosis in early brain injury after subarachnoid hemorrhage.Molecular and cellular biochemistry · 2019Article
- Melatonin Upregulates Nuclear Factor Erythroid-2 Related Factor 2 (Nrf2) and Mediates Mitophagy to Protect Against Early Brain Injury After Subarachnoid Hemorrhage.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- A Comparison of Pathophysiology in Humans and Rodent Models of Subarachnoid Hemorrhage.Frontiers in molecular neuroscience · 2018Review
- Roles of autophagy and endoplasmic reticulum stress in intracerebral hemorrhage-induced secondary brain injury in rats.CNS neuroscience & therapeutics · 2017Article
- Thioredoxin-interacting protein links endoplasmic reticulum stress to inflammatory brain injury and apoptosis after subarachnoid haemorrhage.Journal of neuroinflammation · 2017Article
- Thioredoxin-Interacting Protein Mediates Apoptosis in Early Brain Injury after Subarachnoid Haemorrhage.International journal of molecular sciences · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
background and purposeEndoplasmic reticulum stress triggers apoptotic cascades in neurons of the central nervous system after subarachnoid hemorrhage. The aim of this work was to study the mechanism of neuroprotection conferred by targeting cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in the acute brain injury following subarachnoid hemorrhage.
methodsA total of 172 rats were used. Endovascular perforation induced subarachnoid hemorrhage. Two small interfering RNAs for CHOP were injected 24 hours before hemorrhage induction. At 24 or 72 hours, rats were neurologically evaluated and euthanized. The brains were recovered for molecular biology and histology studies.
resultsWestern blot analysis revealed effective silencing of CHOP associated with suppression of Bim-Caspase-3 apoptotic pathway. Moreover, the antiapoptotic Bcl2 was found upregulated with CHOP siRNA treatment. A reduced number of TUNEL-positive cells in the subcortex and in the hippocampus reflected histological protection. CHOP siRNA treatment ameliorated intracranial sequelae of and improved functional performance.
conclusionsWe conclude that CHOP silencing alleviates early brain injury following subarachnoid hemorrhage via inhibiting apoptosis and that CHOP siRNA treatment has a clinical potential for patients with this type of hemorrhagic stroke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.