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Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis

Authors Chen F, Su X, Lin Z, Lin Y, Yu L, Cai J, Kang D, Hu L

Received 1 May 2017

Accepted for publication 20 June 2017

Published 7 July 2017 Volume 2017:13 Pages 1771—1782


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Wai Kwong Tang

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

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

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