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尿酸通过抗氧化作用对 6-OHDA 诱导的 PC12 细胞损伤的保护作用。

Protective effects of urate against 6-OHDA-induced cell injury in PC12 cells through antioxidant action.

机构信息

Department of Neurology, Second Affiliated Hospital, Soochow University, Suzhou 215004, China.

出版信息

Neurosci Lett. 2012 Jan 11;506(2):175-9. doi: 10.1016/j.neulet.2011.10.075. Epub 2011 Nov 6.

Abstract

There is evidence to support that oxidative stress is increased in Parkinson's disease (PD) and contributes to the degeneration of dopaminergic neurons. Recent research has shown that higher blood urate concentrations have now been linked to decreased risks and progression rates of PD. However, the mechanisms about urate to protect dopaminergic neurons are less clear. Our study investigated the effect of urate on oxidative stress induced by 6-hydroxydopamine (6-OHDA) in neuronal differentiated PC12 cells. We found that urate significantly reduced 6-OHDA-induced lactate dehydrogenas (LDH), malondialdehyde (MDA), and 8-hydroxy-deoxyguanosine (8-OHdG) generation but increased the superoxide dismutase (SOD) activity and glutathione (GSH) levels in the PC12 cells. These results suggested that urate can prevent PC12 cells from oxidative injury induced by 6-OHDA, which may play an important role in the mechanisms underlying the association of high plasma levels of urate with reduced risk and slower progression of PD. Urate treatment could be a potential therapeutic strategy for PD.

摘要

有证据表明,氧化应激在帕金森病(PD)中增加,并导致多巴胺能神经元的退化。最近的研究表明,尿酸浓度升高与 PD 的风险降低和进展速度降低有关。然而,尿酸保护多巴胺能神经元的机制尚不清楚。我们的研究调查了尿酸对神经元分化的 PC12 细胞中 6-羟多巴胺(6-OHDA)诱导的氧化应激的影响。我们发现尿酸显著降低了 6-OHDA 诱导的乳酸脱氢酶(LDH)、丙二醛(MDA)和 8-羟基脱氧鸟苷(8-OHdG)的产生,但增加了 PC12 细胞中超氧化物歧化酶(SOD)活性和谷胱甘肽(GSH)水平。这些结果表明,尿酸可以防止 PC12 细胞免受 6-OHDA 诱导的氧化损伤,这可能在尿酸血浆水平与 PD 的风险降低和进展速度减缓之间的关联的机制中发挥重要作用。尿酸治疗可能是 PD 的一种潜在治疗策略。

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