Open AccessTNF‐α–induced p53 activation induces apoptosis in neurological injury
Author(s) -
Shao Xuefei,
Yang Xiping,
Shen Jun,
Chen Sansong,
Jiang Xiaochun,
Wang Qifu,
Di Qiang
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15333
Subject(s) - apoptosis , traumatic brain injury , tumor necrosis factor alpha , cortex (anatomy) , programmed cell death , biology , necrosis , cerebral cortex , medicine , neuroscience , microbiology and biotechnology , immunology , pathology , biochemistry , psychiatry
It was previously confirmed that the apoptotic and necrotic neurons are found during the acute post‐traumatic period, suggesting the induction of apoptosis after traumatic brain injury (TBI). To further explore the involvement of apoptotic factors in TBI, an apoptosis antibody array was conducted to measure the alterations of apoptotic factors in rat brain cortex after TBI. As a result, the Neurological Severity Scale (NSS) scores after TBI were increased, and the cell morphology of the brain cortex was destructed with increased neuronal apoptosis. Furthermore, the caspase‐3 activity was increased, and the apoptotic‐related factors TNF‐α and p53 were up‐regulated in the brain cortex. More importantly, in vitro experiments demonstrated that down‐regulation of TNF‐α in oxygen‐glucose deprivation/reoxygenation (OGD/R) cells increased cell viability and decreased apoptosis and the p53 expression. These results suggested the involvement of TNF‐α–induced apoptotic signalling pathway by activating p53 in the molecular mechanism of neurological injury.