Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition
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...
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| Format: | Article |
| Language: | English |
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China Science Publishing & Media Ltd.
2024-03-01
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| Series: | Acta Biochimica et Biophysica Sinica |
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| Online Access: | https://www.sciengine.com/doi/10.3724/abbs.2024037 |
| _version_ | 1797208505536479232 |
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| author | Hu Qiang Zhang Rong Dong Xiaoqiao Yang Dingbo Yu Wenhua Du Quan |
| author_facet | Hu Qiang Zhang Rong Dong Xiaoqiao Yang Dingbo Yu Wenhua Du Quan |
| author_sort | Hu Qiang |
| collection | DOAJ |
| description | 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<sub>2</sub>O<sub>2</sub> can induce pyroptosis and inhibit the expressions of ZO-1 and occludin in endothelial cells, which can be blocked by Huperzine A. In addition, the increase in the entry of p65 into the nucleus in endothelial cells can be partly reversed by Huperzine A. Huperzine A may delay the damage of blood-brain barrier in SAH rats by inhibiting oxidative stress-mediated pyroptosis and tight junction protein expression downregulation through the NF-κB pathway. Overall, Huperzine A may have clinical value for treating SAH. |
| first_indexed | 2024-04-24T09:39:52Z |
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| id | doaj.art-6e4fb1a67fd54a888a2f53208b3f923d |
| institution | Directory Open Access Journal |
| issn | 1672-9145 |
| language | English |
| last_indexed | 2024-04-24T09:39:52Z |
| publishDate | 2024-03-01 |
| publisher | China Science Publishing & Media Ltd. |
| record_format | Article |
| series | Acta Biochimica et Biophysica Sinica |
| spelling | doaj.art-6e4fb1a67fd54a888a2f53208b3f923d2024-04-15T07:14:58ZengChina Science Publishing & Media Ltd.Acta Biochimica et Biophysica Sinica1672-91452024-03-015664565610.3724/abbs.202403720d259ccHuperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibitionHu Qiang0Zhang Rong1Dong Xiaoqiao2Yang Dingbo3Yu Wenhua4Du Quan5["Department of Neurosurgery, Affiliated Hangzhou First People’s Hospital, Westlake University School of Medicine, Hangzhou 310000, China","Department of Neurosurgery, Nanjing Medical University Affiliated Hangzhou Hospital, Hangzhou First People’s Hospital, Hangzhou 310000, China"]["Medical Examination Center, Affiliated Hangzhou First People’s Hospital, Westlake University School of Medicine, Hangzhou 310000, China"]["Department of Neurosurgery, Affiliated Hangzhou First People’s Hospital, Westlake University School of Medicine, Hangzhou 310000, China","Department of Neurosurgery, Nanjing Medical University Affiliated Hangzhou Hospital, Hangzhou First People’s Hospital, Hangzhou 310000, China"]["Department of Neurosurgery, Affiliated Hangzhou First People’s Hospital, Westlake University School of Medicine, Hangzhou 310000, China","Department of Neurosurgery, Nanjing Medical University Affiliated Hangzhou Hospital, Hangzhou First People’s Hospital, Hangzhou 310000, China"]["Department of Neurosurgery, Affiliated Hangzhou First People’s Hospital, Westlake University School of Medicine, Hangzhou 310000, China","Department of Neurosurgery, Nanjing Medical University Affiliated Hangzhou Hospital, Hangzhou First People’s Hospital, Hangzhou 310000, China"]["Department of Neurosurgery, Affiliated Hangzhou First People’s Hospital, Westlake University School of Medicine, Hangzhou 310000, China","Department of Neurosurgery, Nanjing Medical University Affiliated Hangzhou Hospital, Hangzhou First People’s Hospital, Hangzhou 310000, China"]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<sub>2</sub>O<sub>2</sub> can induce pyroptosis and inhibit the expressions of ZO-1 and occludin in endothelial cells, which can be blocked by Huperzine A. In addition, the increase in the entry of p65 into the nucleus in endothelial cells can be partly reversed by Huperzine A. Huperzine A may delay the damage of blood-brain barrier in SAH rats by inhibiting oxidative stress-mediated pyroptosis and tight junction protein expression downregulation through the NF-κB pathway. Overall, Huperzine A may have clinical value for treating SAH.https://www.sciengine.com/doi/10.3724/abbs.2024037SAHHuperzine Ablood-brain barrierpyroptosisoxidative stress |
| spellingShingle | Hu Qiang Zhang Rong Dong Xiaoqiao Yang Dingbo Yu Wenhua Du Quan Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition Acta Biochimica et Biophysica Sinica SAH Huperzine A blood-brain barrier pyroptosis oxidative stress |
| title | Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition |
| title_full | Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition |
| title_fullStr | Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition |
| title_full_unstemmed | Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition |
| title_short | Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition |
| title_sort | huperzine a ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition |
| topic | SAH Huperzine A blood-brain barrier pyroptosis oxidative stress |
| url | https://www.sciengine.com/doi/10.3724/abbs.2024037 |
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