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Phytic Acid Protects against 6-Hydroxydopamine-Induced Dopaminergic Neuron Apoptosis in Normal and Iron Excess Conditions in a Cell CultureModel

机译:植酸可在正常和铁过量条件下在细胞培养模型中防御6-羟基多巴胺诱导的多巴胺能神经元凋亡

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摘要

Iron may play an important role in Parkinson’s disease (PD) since it can induce oxidative stress-dependent neurodegeneration. The objective of this study was to determine whether the iron chelator, phytic acid (IP6) can protect against 6-hydroxydopamine- (6-OHDA-) induced apoptosis in immortalized rat mesencephalic dopaminergic cells under normal and iron-excess conditions. Caspase-3 activity was increased about 6-fold after 6-OHDA treatment (compared to control; P \u3c .001) and 30 μmol/L IP6 pretreatment decreased it by 38% (P \u3c .05). Similarly, a 63% protection (P \u3c .001) against 6-OHDA induced DNA fragmentation was observed with IP6 pretreatment. Under iron-excess condition, a 6-fold increase in caspase-3 activity (P \u3c .001) and a 42% increase in DNA fragmentation (P \u3c .05) with 6-OHDA treatment were decreased by 41% (P \u3c .01) and 27% (P \u3c .05), respectively, with 30 μmol/L IP6. Together, our data suggest that IP6 protects against 6-OHDA-induced cell apoptosis in both normal and iron-excess conditions, and IP6 may offer neuroprotection in PD.
机译:铁可能在帕金森氏病(PD)中起重要作用,因为它可以诱导氧化应激依赖性神经变性。这项研究的目的是确定铁螯合剂植酸(IP6)是否可以在正常和铁过量条件下保护永生化大鼠中脑多巴胺能细胞中6-羟基多巴胺-(6-OHDA-)诱导的凋亡。在进行6-OHDA处理后,Caspase-3活性增加了约6倍(与对照相比; P <0.001),而30μmol/ L IP6预处理使Caspase-3活性降低了38%(P <0.05)。类似地,用IP6预处理可观察到63%的保护(P <0.001)对6-OHDA诱导的DNA断裂的保护作用。在铁过量的情况下,6-OHDA处理可使caspase-3活性增加6倍(P <0.001)和使DNA断裂增加42%(P <0.05),降低41%(P \ u3c .01)和27%(P \ u3c .05),IP6为30μmol/ L。总之,我们的数据表明IP6在正常和铁过量条件下均能防御6-OHDA诱导的细胞凋亡,而IP6可能在PD中提供神经保护作用。

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