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Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats
by inhibiting necroptosis
#MMPMID28744127
Chen F
; Su X
; Lin Z
; Lin Y
; Yu L
; Cai J
; Kang D
; Hu L
Neuropsychiatr Dis Treat
2017[]; 13
(?): 1771-1782
PMID28744127
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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.
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