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首页> 外文期刊>CNS neuroscience & therapeutics. >Edaravone Protects HT 22 Neurons from Hsub2/subOsub2/sub‐induced Apoptosis by Inhibiting the MAPK Signaling Pathway
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Edaravone Protects HT 22 Neurons from Hsub2/subOsub2/sub‐induced Apoptosis by Inhibiting the MAPK Signaling Pathway

机译：依达拉奉通过抑制MAPK信号通路保护HT 22神经元免受H 2 O 2 诱导的细胞凋亡

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Summary Aims Oxidative stress is frequently implicated in the pathology of neurodegenerative diseases. This study aimed to investigate the effects and their underlying mechanism(s) of edaravone upon hydrogen peroxide (H2O2)–induced oxidative stress and apoptosis in HT 22 cells, a murine hippocampal neuronal model. Methods HT 22 cells were treated with H2O2 in the presence of various concentrations of edaravone or in its absence. A CCK ‐8 assay, Hoechst 33342 staining, and flow cytometry were used to detect cytotoxicity and apoptosis. In addition, the levels of reactive oxygen species ( ROS ) and the expression of Bcl‐2, Bax, p‐ ERK 1/2, p‐ JNK , and p‐P38 proteins in HT 22 cells were examined. Results Exogenous H2O2 decreased cell viability in a concentration‐dependent manner and was associated with increased apoptosis and ROS production. Moreover, H2O2 significantly activated and upregulated the expression of p‐ ERK 1/2, p‐ JNK , and p‐P38, while edaravon protected HT 22 cells against H2O2‐induced injury by inhibiting the production of ROS and activating the MAPK signaling pathway. Conclusions Our results provide the first evidence that edaravone can protect H2O2‐induced cell injury in HT 22 neurons via its antioxidant action. These findings suggest that edaravone may be useful in the treatment of neurodegenerative disorders in which oxidative stress has been principally implicated.
机译：发明目的氧化应激通常与神经退行性疾病的病理有关。这项研究旨在研究依达拉奉对过氧化氢（H2O2）诱导的小鼠海马神经元模型HT 22细胞的氧化应激和细胞凋亡的影响及其潜在机制。方法在不同浓度的依达拉奉或不存在依达拉奉的情况下，用H2O2处理HT 22细胞。使用CCK-8分析，Hoechst 33342染色和流式细胞仪检测细胞毒性和凋亡。此外，还检测了HT 22细胞中的活性氧（ROS）水平以及Bcl-2，Bax，p-ERK 1/2，p-JNK和p-P38蛋白的表达。结果外源H2O2以浓度依赖性方式降低细胞活力，并与细胞凋亡和ROS产生增加有关。此外，H2O2显着激活并上调了p-ERK 1/2，p-JNK和p-P38的表达，而edaravon通过抑制ROS的产生并激活MAPK信号通路来保护HT 22细胞免受H2O2诱导的伤害。结论我们的结果提供了第一个证据，表明依达拉奉可通过其抗氧化作用来保护H2O2诱导的HT 22神经元细胞损伤。这些发现表明，依达拉奉在治疗主要涉及氧化应激的神经退行性疾病中可能是有用的。

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