Premium
The involvement of nuclear factor‐κB in astroprotection against ischemia‐reperfusion injury by ischemia‐preconditioned neurons
Author(s) -
Wu XiaoMei,
Qian Christopher,
Jiang Fei,
Bao YuXin,
Qian ZhongMing,
Ke Ya
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30168
Subject(s) - oxidative stress , reactive oxygen species , downregulation and upregulation , erythropoietin , nf κb , viability assay , antioxidant , tumor necrosis factor alpha , chemistry , ischemia , pharmacology , reperfusion injury , neuron , microbiology and biotechnology , signal transduction , biology , cell , medicine , biochemistry , immunology , endocrinology , neuroscience , gene
Ischemic preconditioned (IP) neurons protect astrocytes against ischemia/reperfusion (I/R)‐induced injury by inhibiting oxidative stress. However, the relevant mechanisms are unknown. Based on the role of nuclear factor‐κB (NF‐κB) in cell survival and adaption to oxidative stress, we hypothesized that NF‐κB might be associated with astroprotection induced by IP neurons via upregulation of antioxidant enzymes. Here, we investigated the effects of IP neurons on NF‐κB activation, cell viability, reactive oxygen species (ROS), expression of antioxidant enzymes, erythropoietin (EPO), and tumor necrosis factor α (TNF‐α), in the presence or absence of BAY11‐7082 (an NF‐κB inhibitor), anti‐EPO, and anti‐TNF‐α antibodies, in astrocytes treated with or without I/R. We found that IP neurons could keep NF‐κB activation at a relatively higher but beneficial level, and in turn, upregulated the activity of antioxidant enzymes and hence enhanced cell viability and reduced ROS in I/R treated astrocytes. The results collectively indicated that IP neurons are able to significantly inhibit the I/R‐induced NF‐κB overactivation, probably via EPO and TNF‐α, being essential for IP neuron‐induced astroprotection under the conditions of I/R. We concluded that NF‐κB‐mediated antioxidative stress is one of the mechanisms by which IP neurons protect astrocytes against I/R injury.