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- Title
Role of necroptosis in early brain injury after subarachnoid hemorrhage in rats.
- Authors
WANG Gang; AN Ji-yang; SONG Jin-ning; SUN Lei-tao; LI Dan-dong; MA Xu-dong; ZHANG Bin-fei
- Abstract
Objective To investigate the activation of necroptosis pathway and explore the role and molecular mechanism of necroptosis in early brain injury after subarachnoid hemorrhage (SAH). Methods Forty adult male SD rats were divided into four groups ( n = 10 in each): sham, SAH, and SAH treatment plus Nec-1 or dimethyl sulfoxide (DMSO) . SAH model was established by endovascular perforation technique. In SAH+Nec-1 and SAH+ DMSO groups, Nec-1 or DMSO was injected intracerebroventsicularly 30 min prior to SAH establishment. Animals were then sacrificed at 24 h after modeling in each group. The neurological severity scores and brain water content were determined; immunohistochemical method was used in detecting the expression of receptor interacting protein 3 (RIP3). Results Neurological dysfunction, the number of necrotic neuronal cells, brain water content and the expression of RIP3 were significantly increased in the brain tissues of SAH rats (P<0.01). Neurological dysfunction, the number of necrotic neuronal cells, brain water content and the expression of RIP3 were significantly reduced after Nec-1 treatment (P<0.01). Conclusion Necroptoiis is activated and involved in the pathophysiological mechanism of early brain injury after SAH. RIP3 may play a crucial role in necroptosis pathway. Inhibiting necroptosis may be of great importance for protecting neuronal cells and reducing edema in early brain injury after SAH.
- Subjects
APOPTOSIS; BRAIN injuries; SUBARACHNOID hemorrhage; LABORATORY rats; DIMETHYL sulfoxide; NEUROLOGY
- Publication
Journal of Xi'an Jiaotong University (Medical Sciences), 2013, Vol 34, Issue 6, p722
- ISSN
1671-8259
- Publication type
Article
- DOI
10.7652/jdyxb201306005