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 surv...
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https://www.riss.kr/link?id=O111279652
2021년
-
0021-9541
1097-4652
SCI;SCIE;SCOPUS
학술저널
4515-4527 [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
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 surv...
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.
Our results collectively indicated that IP neurons are able to significantly inhibit the ischemia/reperfusion (I/R)‐induced nuclear factor κB (NF‐κB) over‐activation, probably via erythropoietin (EPO) and tumor necrosis factor α (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.