6-Hydroxydopamine-induced decrease in dopaminergic neurons is avoided by effusol and dehydroeffusol, unique phenanthrenes of Juncus effusus

IF 2.4 Q3 NUTRITION & DIETETICS
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Abstract

Background

Excess influx of extracellular Zn2+ into nigral dopaminergic neurons play a crucial role for 6-hydroxydopamine (6-OHDA)-induced Parkinson's disease in rats. On the basis of neurodegeneration by Zn2+ dysregulation, we aimed to clarify the effect of effusol and dehydroeffusol, unique phenanthrenes from Juncus effusus on dopaminergic degeneration.

Methods

The decrease in dopaminergic neurons was assessed by tyrosine hydroxylase immunostaining 14 days after 6-OHDA injection into the substantia nigra pars compacta (SNpc) of rats.

Results

The decrease in dopaminergic neurons induced by 6-OHDA was avoided by co-injection of 1-naphthyl acetyl spermine (NASPM), a selective blocker of Zn2+-permeable GluR2-lacking AMPA receptors, which blocked the increase in intracellular Zn2+, supporting the involvement of Zn2+ dysregulation in dopaminergic degeneration. Moreover, either effusol or dehydroeffusol was co-injected with 6-OHDA into the SNpc. The decrease in dopaminergic neurons was avoided by effusol and dehydroeffusol. The increases in intracellular Zn2+ and H2O2 in the SNpc induced by 6-OHDA were also avoided by effusol and dehydroeffusol.

Conclusions

The present study first indicates that effusol and dehydroeffusol avoid the decrease in dopaminergic neurons in the SNpc via reducing production of reactive oxygen species induced by intracellular Zn2+ dysregulation after injection of 6-OHDA into the rat SNpc. It is likely that effusol and dehydroeffusol serve as nutraceutical components to protect dopaminergic degeneration, perhaps via regulating presynaptic excitation of glutamatergic neurons in the SNpc.

多巴胺能神经元的6-羟基多巴胺诱导的减少可被流苏醇和脱氢流苏醇(流苏中特有的菲类化合物)所避免
背景 细胞外Zn2+过度流入黑质多巴胺能神经元对6-羟基多巴胺(6-OHDA)诱导的大鼠帕金森病起着关键作用。在Zn2+失调导致神经变性的基础上,我们旨在阐明从黄花菜中提取的独特菲酚--黄花菜醇和脱氢黄花菜醇对多巴胺能变性的影响。方法在大鼠黑质(SNpc)注射6-OHDA 14天后,用酪氨酸羟化酶免疫染色法评估多巴胺能神经元的减少。结果 同时注射1-萘基乙酰精胺(NASPM)可避免6-OHDA诱导的多巴胺能神经元的减少,NASPM是一种选择性阻断Zn2+渗透性GluR2-lacking AMPA受体的药物,可阻断细胞内Zn2+的增加,支持Zn2+失调参与多巴胺能变性。此外,将泡腾醇和脱氢泡腾醇与6-OHDA同时注射到SNpc。叶黄素和脱氢叶黄素可避免多巴胺能神经元的减少。结论本研究首先表明,向大鼠SNpc注射6-OHDA后,泡腾醇和去氢泡腾醇能减少细胞内Zn2+失调引起的活性氧的产生,从而避免了SNpc中多巴胺能神经元的减少。泡腾醇和脱氢泡腾醇很可能是保护多巴胺能变性的营养保健成分,也许是通过调节SNpc中谷氨酸能神经元突触前兴奋来实现的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
PharmaNutrition
PharmaNutrition Agricultural and Biological Sciences-Food Science
CiteScore
5.70
自引率
3.10%
发文量
33
审稿时长
12 days
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