首页> 外文期刊>International Journal of Molecular Sciences >Neuroprotective Effects of Erucin against 6-Hydroxydopamine-Induced Oxidative Damage in a Dopaminergic-like Neuroblastoma Cell Line
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Neuroprotective Effects of Erucin against 6-Hydroxydopamine-Induced Oxidative Damage in a Dopaminergic-like Neuroblastoma Cell Line

机译:尤里霉素对多巴胺能样神经母细胞瘤细胞系中6-羟基多巴胺诱导的氧化损伤的神经保护作用。

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Oxidative stress (OS) contributes to the cascade leading to the dysfunction or death of dopaminergic neurons during Parkinson’s disease (PD). A strategy to prevent the OS of dopaminergic neurons may be the use of phytochemicals as inducers of endogenous antioxidants and phase 2 enzymes. In this study, we demonstrated that treatment of the dopaminergic-like neuroblastoma SH-SY5Y cell line with isothiocyanate erucin (ER), a compound of cruciferous vegetables, resulted in significant increases of both total glutathione (GSH) levels and total antioxidant capacity at the cytosolic level. The increase of GSH levels was associated with an increase in the resistance of SH-SY5Y cells to neuronal death, in terms of apoptosis, induced by 6-hydroxydopamine (6-OHDA). The pretreatment of SH-SY5Y cells with ER was also shown to prevent the redox status impairment, in terms of intracellular ROS and O2•− formation, and loss of mitochondrial membrane potential, early events that are initiators of the apoptotic process, induced by 6-OHDA. Last, the antiapoptotic and antioxidant effects of ER were abolished by buthionine sulfoximine, supporting the main role of GSH in the neuroprotective effects recorded by ER. These results suggest that ER may prevent the oxidative damage induced by 6-OHDA.
机译:在帕金森氏病(PD)期间,氧化应激(OS)导致级联反应,导致多巴胺能神经元功能障碍或死亡。预防多巴胺能神经元OS的策略可能是使用植物化学物质作为内源性抗氧化剂和2相酶的诱导剂。在这项研究中,我们证明了用十字花科蔬菜的化合物异硫氰酸酯芥子酸酯(ER)处理多巴胺能样神经母细胞瘤SH-SY5Y细胞系会导致总谷胱甘肽(GSH)水平和总抗氧化能力显着增加。胞浆水平。 GSH水平的增加与SH-SY5Y细胞对6-羟基多巴胺(6-OHDA)诱导的神经元死亡的抗性增加有关。从细胞内ROS和O 2 •-的形成以及线粒体膜的丧失方面来看,ER预处理SH-SY5Y细胞还可以防止氧化还原状态受损。潜在的早期事件,是由6-OHDA诱导的凋亡过程的发起者。最后,丁硫氨酸亚砜亚胺消除了ER的抗凋亡和抗氧化作用,支持了GSH在ER记录的神经保护作用中的主要作用。这些结果表明,ER可以防止6-OHDA引起的氧化损伤。

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