Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis
Fuxiang Chen,1 Xingfen Su,1 Zhangya Lin,1 Yuanxiang Lin,1 Lianghong Yu,1 Jiawei Cai,1 Dezhi Kang,1 Liwen Hu2 1Department of Neurosurgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China; 2Department of Pathology, The First Affiliated Hospital&...
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Dove Medical Press
2017
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oai:doaj.org-article:663b2558ed94426da38b5e329cfd5d8f2021-12-02T02:51:40ZNecrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis1178-2021https://doaj.org/article/663b2558ed94426da38b5e329cfd5d8f2017-07-01T00:00:00Zhttps://www.dovepress.com/necrostatin-1-attenuates-early-brain-injury-after-subarachnoid-hemorrh-peer-reviewed-article-NDThttps://doaj.org/toc/1178-2021Fuxiang Chen,1 Xingfen Su,1 Zhangya Lin,1 Yuanxiang Lin,1 Lianghong Yu,1 Jiawei Cai,1 Dezhi Kang,1 Liwen Hu2 1Department of Neurosurgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China; 2Department of Pathology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China Abstract: Necroptosis is programmed cell death that has been recently proposed and reported to be involved in several neurologic diseases. However, the role of necroptosis in early brain injury after subarachnoid hemorrhage (SAH) is still unknown. The purpose of this study was to investigate whether necroptosis was involved in SAH-induced early brain injury, and to assess the possible neuroprotective effect of necrostatin-1 using an endovascular perforation rat model of SAH. Our results showed that the expression levels of necroptosis-related proteins including RIP1, RIP3 and MLKL in the basal cortex all increased at 3 hours after SAH (P<0.05) and peaked at 48 hours after SAH (P<0.05). However, they were greatly reduced after treatment with necrostatin-1 (P<0.05). Concurrently, neurologic outcomes were significantly improved after necrostatin-1 treatment (P<0.05). Furthermore, brain edema, blood–brain barrier disruption, necrotic cell death and neuroinflammation were also greatly inhibited after necrostatin-1 treatment. These results indicate that necroptosis is an important mechanism of cell death involved in the early brain injury after experimental SAH. Necrostatin-1 perhaps can serve as a promising neuroprotective agent for SAH treatment. Keywords: subarachnoid hemorrhage, necroptosis, receptor-interacting protein 1, cell death, neuroprotectionChen FSu XLin ZLin YYu LCai JKang DHu LDove Medical PressarticleSubarachnoid hemorrhageNecroptosis;Necrostatin-1Cell deathNeuroprotectionNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571Neurology. Diseases of the nervous systemRC346-429ENNeuropsychiatric Disease and Treatment, Vol Volume 13, Pp 1771-1782 (2017) |
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Subarachnoid hemorrhage Necroptosis;Necrostatin-1 Cell death Neuroprotection Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 |
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Subarachnoid hemorrhage Necroptosis;Necrostatin-1 Cell death Neuroprotection Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 Chen F Su X Lin Z Lin Y Yu L Cai J Kang D Hu L Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis |
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Fuxiang Chen,1 Xingfen Su,1 Zhangya Lin,1 Yuanxiang Lin,1 Lianghong Yu,1 Jiawei Cai,1 Dezhi Kang,1 Liwen Hu2 1Department of Neurosurgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China; 2Department of Pathology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China Abstract: Necroptosis is programmed cell death that has been recently proposed and reported to be involved in several neurologic diseases. However, the role of necroptosis in early brain injury after subarachnoid hemorrhage (SAH) is still unknown. The purpose of this study was to investigate whether necroptosis was involved in SAH-induced early brain injury, and to assess the possible neuroprotective effect of necrostatin-1 using an endovascular perforation rat model of SAH. Our results showed that the expression levels of necroptosis-related proteins including RIP1, RIP3 and MLKL in the basal cortex all increased at 3 hours after SAH (P<0.05) and peaked at 48 hours after SAH (P<0.05). However, they were greatly reduced after treatment with necrostatin-1 (P<0.05). Concurrently, neurologic outcomes were significantly improved after necrostatin-1 treatment (P<0.05). Furthermore, brain edema, blood–brain barrier disruption, necrotic cell death and neuroinflammation were also greatly inhibited after necrostatin-1 treatment. These results indicate that necroptosis is an important mechanism of cell death involved in the early brain injury after experimental SAH. Necrostatin-1 perhaps can serve as a promising neuroprotective agent for SAH treatment. Keywords: subarachnoid hemorrhage, necroptosis, receptor-interacting protein 1, cell death, neuroprotection |
format |
article |
author |
Chen F Su X Lin Z Lin Y Yu L Cai J Kang D Hu L |
author_facet |
Chen F Su X Lin Z Lin Y Yu L Cai J Kang D Hu L |
author_sort |
Chen F |
title |
Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis |
title_short |
Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis |
title_full |
Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis |
title_fullStr |
Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis |
title_full_unstemmed |
Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis |
title_sort |
necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis |
publisher |
Dove Medical Press |
publishDate |
2017 |
url |
https://doaj.org/article/663b2558ed94426da38b5e329cfd5d8f |
work_keys_str_mv |
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