Open AccessNecrostatin-1 decreases necroptosis and inflammatory markers after intraventricular hemorrhage in mice
Author(s) -
Chang Liu,
Yi Cao,
Hao-Xiang Wang,
Liang Zhao,
Yaxing Chen,
Kunhong Zhong,
Gaowei Li,
Guoqing Wang,
Keru Huang,
Aiping Tong,
Liangxue Zhou
Publication year - 2022
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.339488
Subject(s) - necroptosis , ventricle , inflammation , medicine , programmed cell death , apoptosis , tumor necrosis factor alpha , necrosis , microbiology and biotechnology , anesthesia , biology , biochemistry
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.