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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >1-Methyl-4-phenyl-pyridinium ion-induced oxidative stress, c-Jun phosphorylation and DNA fragmentation factor-45 cleavage in SK-N-SH cells are averted by selegiline.
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1-Methyl-4-phenyl-pyridinium ion-induced oxidative stress, c-Jun phosphorylation and DNA fragmentation factor-45 cleavage in SK-N-SH cells are averted by selegiline.

机译:司来吉兰可避免SK-N-SH细胞中1-甲基-4-苯基吡啶鎓离子诱导的氧化应激,c-Jun磷酸化和DNA断裂因子-45裂解。

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摘要

Parkinson's disease is a progressive neurodegenerative disorder, associated with the selective loss of dopaminergic neurons in the substantia nigra pars compacta. Recent studies have shown that c-Jun-N terminal kinase pathways might be involved in the oxidative stress-induced neuronal demise. In addition, there are several studies demonstrating that selegiline protects neural cell degeneration. In view of the above, the toxic effects of MPP(+) and the protective roles of selegiline were studied in cultures of human neuroblastoma (SK-N-SH) cell lines in the present study. MPP(+) significantly decreased cell viability but increased reactive oxygen species formation and lipid peroxidation, and the said effects were attenuated by selegiline. MPP(+) did not change the total levels of c-Jun but enhanced phosphorylation of c-Jun at Ser73 and cleavage of DNA fragmentation factor 45, which were diminished by selegiline. MPP(+)-treated SK-N-SH cells exhibited an irregularly shaped nuclear chromatin or DNA fragmentation, which was abolished by selegiline. These data suggest that c-Jun-N terminal kinase pathways are involved in oxidative stress-induced dopaminergic neuronal degeneration and pretreatment with selegiline affords neuroprotection by inhibiting these cell death-signaling pathways.
机译:帕金森氏病是一种进行性神经退行性疾病,与黑质致密部中的多巴胺能神经元选择性丢失有关。最近的研究表明,c-Jun-N末端激酶途径可能与氧化应激诱导的神经元死亡有关。另外,有几项研究表明司来吉兰可保护神经细胞变性。有鉴于此,本研究在人成神经细胞瘤(SK-N-SH)细胞系培养物中研究了MPP(+)的毒性作用和司来吉兰的保护作用。 MPP(+)大大降低了细胞活力,但增加了活性氧的形成和脂质过氧化作用,司来吉兰减弱了上述作用。 MPP(+)不会改变c-Jun的总水平,但会增强Ser-73上c-Jun的磷酸化和DNA断裂因子45的裂解,这被司来吉兰所减弱。 MPP(+)处理的SK-N-SH细胞显示出不规则形状的核染色质或DNA片段,其被司来吉兰废除。这些数据表明,c-Jun-N末端激酶途径参与了氧化应激诱导的多巴胺能神经元变性,司来吉兰的预处理通过抑制这些细胞死亡信号通路而提供了神经保护作用。

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