Necrostatin-1 decreases necroptosis and inflammatory markers after intraventricular hemorrhage in mice

Necrostatin-1, an inhibitor of necroptosis, can effectively inhibit necrotic apoptosis in neurological diseases, which results in the inhibition of inflammation, endoplasmic reticulum stress, and reactive oxygen species production and substantial improvement of neurological function. However, the ef...

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Bibliographic Details
Published in:Neural regeneration research 2022-12, Vol.17 (12), p.2710-2716
Main Authors: Liu, Chang, Cao, Yi, Wang, Hao-Xiang, Zhao, Long, Chen, Ya-Xing, Zhong, Kun-Hong, Li, Gao-Wei, Wang, Guo-Qing, Huang, Ke-Ru, Tong, Ai-Ping, Zhou, Liang-Xue
Format: Article
Language:English
Subjects:
Cytokines
ependymal cilia
hydrocephalus
inflammation
intraventricular hemorrhage
microglia
mlkl
necroptosis
necrostatin-1
rip1
rip3
Kinases
Reactive oxygen species
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Summary:Necrostatin-1, an inhibitor of necroptosis, can effectively inhibit necrotic apoptosis in neurological diseases, which results in the inhibition of inflammation, endoplasmic reticulum stress, and reactive oxygen species production and substantial improvement of neurological function. However, the effects of necrostatin-1 on intraventricular hemorrhage (IVH) remain unknown. In this study, we established a mouse model of IVH by injecting autologous blood into the lateral ventricle of the brain. We also injected necrostatin-1 into the lateral ventricle one hour prior to IVH induction. We found that necrostatin-1 effectively reduced the expression levels of the necroptosis markers receptor-interacting protein kinase (RIP)1, RIP3, mixed lineage kinase domain-like protein (MLKL), phosphorylated (p)-RIP3, and p-MLKL and the levels of interleukin-1β , interleukin-6, and tumor necrosis factor-α in the surrounding areas of the lateral ventricle. However, necrostatin-1 did not reduce ependymal ciliary injury or brain water content. These findings suggest that necrostatin-1 can prevent local inflammation and microglial activation induced by IVH but does not greatly improve prognosis.
ISSN:1673-5374
1876-7958
DOI:10.4103/1673-5374.339488