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首页> 外文期刊>Redox report: communications in free radical research >Possible role of NF-κB in Bcl-X_L protection against hydrogen peroxide-induced PC12 cell death
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Possible role of NF-κB in Bcl-X_L protection against hydrogen peroxide-induced PC12 cell death

机译：NF-κB在Bcl-X_L预防过氧化氢诱导PC12细胞死亡中的可能作用

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摘要

Bcl-X_L, a mitochondrial membrane protein, blocks apoptosis induced by a wide array of death signals. In spite of extensive research, the molecular milieu that characterizes the anti-apoptotic function of Bcl-X_L is complex and not fully clarified. In the present work, we have investigated the role of Bcl-X_L in protecting against oxidative death induced by H_2O_2 in cultured rat pheochromocytoma (PC12) cells. PC12 cells exposed to H_2O_2 underwent apoptotic cell death as determined by internucleosomal DNA fragmentation and an increased pro-apoptotic Bax to anti-apoptotic Bcl-X_L ratio. Moreover, stable transfection with the bcl-X_L gene rescued PC12 cells from apoptotic death caused by H_2O_2. PC12 cells overexpressing bcl-X_L exhibited relatively high constitutive transcriptional as well as DNA binding activities of NF-κB, compared with the vector-transfected control cells. Addition of NF-κB inhibitors, such as parthenolide and N-tosyl-L-phenylalanine chloromethyl ketone, to the media aggravated H_2O_2-induced oxidative cell death. PC12 cells transfected with bcl-X_L exhibited higher levels of the heme oxygenase-1, which may confer these cells protection against oxidative stress. These results suggest that the redox-sensitive transcription factor NF-κB may play a role in bcl-X_L-mediated protection against oxidative cell death.
机译：Bcl-X_L是一种线粒体膜蛋白，可阻断多种死亡信号诱导的细胞凋亡。尽管进行了广泛的研究，但表征Bcl-X_L的抗凋亡功能的分子环境仍然复杂且尚未完全阐明。在目前的工作中，我们已经研究了Bcl-X_L在防止H_2O_2在培养的大鼠嗜铬细胞瘤（PC12）细胞中诱导的氧化死亡中的作用。暴露于H_2O_2的PC12细胞通过核小体间DNA片段化和促凋亡的Bax与抗凋亡Bcl-X_L比率增加而凋亡。此外，bcl-X_L基因的稳定转染使PC12细胞免于H_2O_2引起的细胞凋亡。与载体转染的对照细胞相比，过表达bcl-X_L的PC12细胞表现出较高的NF-κB组成型转录和DNA结合活性。在培养基中添加NF-κB抑制剂（如小白菊内酯和N-甲苯磺酰基-L-苯丙氨酸氯甲基酮）会加剧H_2O_2诱导的氧化细胞死亡。用bcl-X_L转染的PC12细胞表现出更高水平的血红素加氧酶-1，这可能赋予这些细胞抗氧化应激的保护作用。这些结果表明，氧化还原敏感的转录因子NF-κB可能在bcl-X_L介导的抗氧化细胞死亡的保护中起作用。

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