The involvement of nuclear factor‐κB in astroprotection against ischemia‐reperfusion injury by ischemia‐preconditioned neurons,Journal of Cellular Physiology

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The involvement of nuclear factor‐κB in astroprotection against ischemia‐reperfusion injury by ischemia‐preconditioned neurons
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2021-01-14 , DOI: 10.1002/jcp.30168
Xiao-Mei Wu _{1,

2} , Christopher Qian ₂ , Fei Jiang ₁ , Yu-Xin Bao ₃ , Zhong-Ming Qian _{1,

4} , Ya Ke ₂

Affiliation

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.

中文翻译：

核因子-κB参与缺血预处理神经元对缺血再灌注损伤的星体保护

缺血预调节（IP）神经元通过抑制氧化应激来保护星形胶质细胞免受缺血/再灌注（I/R）诱导的损伤。然而，相关机制尚不清楚。基于核因子-κB (NF-κB) 在细胞存活和氧化应激适应中的作用，我们假设 NF-κB 可能与 IP 神经元通过抗氧化酶上调诱导的星形保护有关。在这里，我们研究了 IP 神经元在存在或存在的情况下对 NF-κB 激活、细胞活力、活性氧 (ROS)、抗氧化酶、促红细胞生成素 (EPO) 和肿瘤坏死因子 α (TNF-α) 表达的影响。在用或不用 I/R 处理的星形胶质细胞中不存在 BAY11-7082（一种 NF-κB 抑制剂）、抗 EPO 和抗 TNF-α 抗体。我们发现 IP 神经元可以将 NF-κB 激活保持在相对较高但有益的水平，进而上调抗氧化酶的活性，从而增强 I/R 处理的星形胶质细胞的细胞活力并减少 ROS。结果总体表明，IP 神经元能够显着抑制 I/R 诱导的 NF-κB 过度激活，可能是通过 EPO 和 TNF-α，这对于 I/R 条件下 IP 神经元诱导的星体保护至关重要。我们得出结论，NF-κB 介导的抗氧化应激是 IP 神经元保护星形胶质细胞免受 I/R 损伤的机制之一。

更新日期：2021-03-23

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