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Open AccessDOI: 10.3724/abbs.2024037Original Research

Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition

🇨🇳 Original Chinese Title: Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition

Qiang Hu¹,Rong Zhang¹,Xiaoqiao Dong¹,Dingbo Yang¹,Quan Du¹,Wenhua Yu¹

Department of Neurosurgery, The Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou 310000, China

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Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition
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Published In
Acta Biochimica et Biophysica Sinica
Published:2024Edition:Vol. 56, Issue 4 • pp. 645-656Citation:Qiang Hu et al. (2024), Acta Biochimica et Biophysica Sinica
Impact FactorPremier Chinese Biomedical Journal indexed in SinoBioData: Acta Biochimica et Biophysica Sinica (生物化学与生物物理学报).
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Key Takeaways & Executive Findings

  • • Huperzine A attenuates neurological deficits after spontaneous subarachnoid hemorrhage by inhibiting endothelial cell pyroptosis. • The study identifies endothelial cell pyroptosis as a key therapeutic target in subarachnoid hemorrhage. • Huperzine A may offer a novel neuroprotective strategy for patients with subarachnoid hemorrhage. • The corrigendum ensures accurate attribution of authorship and affiliations for the original research.
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Abstract

This is a corrigendum to the original article. The original article reported that Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition. The corrigendum corrects errors in the author list and affiliations. The corrected authors and affiliations are provided.

1. Introduction

Spontaneous subarachnoid hemorrhage (SAH) is a devastating cerebrovascular event with high morbidity and mortality. Early brain injury, including endothelial cell dysfunction and neuroinflammation, contributes to poor outcomes. Pyroptosis, a pro-inflammatory form of programmed cell death, has been implicated in the pathogenesis of SAH. Huperzine A, an alkaloid derived from the Chinese club moss Huperzia serrata, has demonstrated neuroprotective properties in various neurological disorders. This study aimed to investigate whether Huperzine A could ameliorate neurological deficits after SAH by inhibiting endothelial cell pyroptosis.

The original article presented findings that Huperzine A treatment significantly reduced neurological deficits and attenuated endothelial cell pyroptosis in a mouse model of SAH. The corrigendum addresses errors in the author list and affiliations to ensure proper credit and transparency.

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Cite This Research Paper
Qiang Hu, Rong Zhang, Xiaoqiao Dong, Dingbo Yang, Quan Du, Wenhua Yu (2026). Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition. Acta Biochimica et Biophysica Sinica. https://doi.org/10.3724/abbs.2024037
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Frequently Asked Questions

What is the main finding of the study on Huperzine A and subarachnoid hemorrhage?

The study found that Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage by inhibiting endothelial cell pyroptosis.

What is the significance of endothelial cell pyroptosis in subarachnoid hemorrhage?

Endothelial cell pyroptosis is a key pathological mechanism contributing to early brain injury and neurological deficits after subarachnoid hemorrhage, making it a potential therapeutic target.

What corrections were made in the corrigendum?

The corrigendum corrected errors in the author list and affiliations of the original article to ensure accurate attribution.

Where was the research conducted?

The research was conducted at the Department of Neurosurgery, The Affiliated Hangzhou Hospital of Nanjing Medical University, and Affiliated Hangzhou First People’s Hospital, School of Medicine, Westlake University, Hangzhou, China.

What is the DOI of the original article?

The DOI of the original article is 10.3724/abbs.2024037.

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