ArticleActa biochimica et biophysica Sinica2024
Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition.
Article in Acta biochimica et biophysica Sinica, 2024. 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 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- Huperzine A improves neurological function in mice with intracerebral hemorrhage by alleviating neuroinflammation and ferroptosis.Scientific reports · 2026Article
- Integrated Transcriptomic and Proteomic Analysis Elucidates the Mechanisms of Huperzine A Injection Against Cerebral Ischemia/Reperfusion Injury.Drug design, development and therapy · 2026Article
- Succinate accumulation induces pyroptosis and mitochondrial damage via the inhibition of ATP5F1D in HUVECs.Acta biochimica et biophysica Sinica · 2025Article
- Investigating the Potential Therapeutic Targeting of the JAK-STAT Pathway in Cerebrovascular Diseases: Opportunities and Challenges.Molecular neurobiology · 2025Review
- Retinoic acid-inducible gene-I aggravates neuroinflammation in early brain injury after subarachnoid hemorrhage through mediating brain microvascular endothelial cell pyroptosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Single-cell sequencing reveals intracranial microvasculature-derived CXCL12 promotes CD8Journal of neuroinflammation · 2025Article
- Review
- Utility of Serum Occludin as a Prognostic Biomarker of Severe Traumatic Brain Injury and Mediation Role of Acute Lung Injury: A Two-Center Prospective Cohort Study.International journal of general medicine · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spontaneous subarachnoid hemorrhage (SAH) is a kind of hemorrhagic stroke which causes neurological deficits in survivors. Huperzine A has a neuroprotective effect, but its role in SAH is unclear. Therefore, we explore the effect of Huperzine A on neurological deficits induced by SAH and the related mechanism. In this study, Evans blue assay, TUNEL staining, immunofluorescence, western blot analysis, and ELISA are conducted. We find that Huperzine A can improve neurological deficits and inhibit the apoptosis of nerve cells in SAH rats. Huperzine A treatment can improve the upregulation of brain water content, damage of blood-brain barrier, fibrinogen and matrix metalloprotein 9 expressions and the downregulation of ZO-1 and occludin expressions induced by SAH. Huperzine A inhibit the expressions of proteins involved in pyroptosis in endothelial cells in SAH rats. The increase in MDA content and decrease in SOD activity in SAH rats can be partly reversed by Huperzine A. The ROS inducer H
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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.