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Antioxidant N-Acetylcysteine Blocks Nerve Growth Factor-Induced H_2O_2/ERK Signaling in PC12 Cells

机译:抗氧化剂N-乙酰琥珀嵌段阻断神经生长因子诱导的PC12细胞中的H_2O_2 / ERK信号传导

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We investigated whether H_2O_2, superoxide, and ERK participate in nerve growth factor (NGF)-induced signaling cascades and whether antioxidant N-acetylcysteine (NAC) regulates these NGF-induced responses. PC12 cells were cultured in medium containing NGF or vehicle with or without NAC pretreatment, and the intracellular H_2O_2 and superoxide levels and the amount of phosphorylated ERK were evaluated by flow cytometry and Western blotting, respectively. We found that NGF increased intracellular H_2O_2 concentration and activated ERK but failed to affect intracellular superoxide level. Moreover, NAC counteracted these NGF-induced responses. These findings demonstrate that NAC blocks the NGF-induced H_2O_2/ERK signaling in PC12 cells.
机译:我们研究了H_2O_2,超氧化物和ERK是否参与神经生长因子(NGF)引起的信号级联,以及抗氧化剂N-乙酰半胱氨酸(NAC)调节这些NGF诱导的反应。在含有NGF或载体的培养基中培养PC12细胞,或没有NAC预处理,通过流式细胞术和Western印迹评估细胞内H_2O_2和超氧化物水平和磷酸化ERK的量。我们发现NGF增加细胞内H_2O_2浓度和活化的ERK,但未影响细胞内超氧化物水平。此外,NAC抵消了这些NGF诱导的反应。这些发现表明NAC阻断了PC12细胞中的NGF诱导的H_2O_2 / ERK信号。

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