ArticleBMC neurology2017
Neuroprotective effect of neuroserpin in non-tPA-induced intracerebral hemorrhage mouse models.
Article in BMC neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Neuroserpin and Extracellular Vesicles in Ischemic Stroke: Partners in Neuroprotection?Aging and disease · 2024Review
- The probable role of tissue plasminogen activator/neuroserpin axis in Alzheimer's disease: a new perspective.Acta neurologica Belgica · 2024Review
- Molecular, Pathological, Clinical, and Therapeutic Aspects of Perihematomal Edema in Different Stages of Intracerebral Hemorrhage.Oxidative medicine and cellular longevity · 2022Review
- The plasminogen activating system in the pathogenesis of Alzheimer's disease.Neural regeneration research · 2021Review
- Deficiency in Neuroserpin Exacerbates CoClFrontiers in pharmacology · 2021Article
- The Neuroprotective Role of Neuroserpin in Ischemic and Hemorrhagic Stroke.Current neuropharmacology · 2021Review
- Serine Proteases and Chemokines in Neurotrauma: New Targets for Immune Modulating Therapeutics in Spinal Cord Injury.Current neuropharmacology · 2021Review
- Neuroserpin expression during human brain development and in adult brain revealed by immunohistochemistry and single cell RNA sequencing.Journal of anatomy · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe neuroprotective effects of neuroserpin (NSP) have been well documented in both patients and animal models with cerebral ischemia; however, have never been investigated in hemorrhagic stroke. The aim of this study is to verify the neuroprotection of NSP in the non-tPA-induced intracerebral hemorrhage (ICH) mouse model.
methodsC57BL/6J male mice (n = 198) were involved in this study. ICH models were established with infusion of autologous blood into the brain parenchyma. We then detected NSP expression in ICH brains by morphological methods and western blotting analysis. We measured the brain water content and detected blood-brain barrier (BBB) permeability to verify the neuroprotective effects of NSP.
resultsWe found that NSP protein expression was upregulated in ICH models, with a peak at 48 h after ICH induction. NSP local administration reduced the brain edema and the BBB permeability in ICH models. The neurological deficits were also ameliorated. Thus, the neuroprotection of NSP in ICH state was confirmed. Additionally, we also found that the distribution pattern of occludin-expressing cells was obviously changed by the ICH procedure but partly recovered after NSP administration. This finding indicated that protecting and/or repairing the injured vascular endothelial cells may be a potential mechanism involved in NSP neuroprotection, which needs further verification.
conclusionsOur results supported the fact that NSP may be considered as a potential therapy for ICH for the neuroprotective effects including amelioration of the edema.
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