Ginsenoside Rd and ginsenoside Re offer neuroprotection in a novel model of Parkinson's disease.

American journal of neurodegenerative disease Pub Date : 2016-03-01 eCollection Date: 2016-01-01
Xinmu Zhang, Yingzi Wang, Cheng Ma, Yan Yan, Yang Yang, Xin Wang, Wolf-Dieter Rausch
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Abstract

Ginsenosides are the main active constituents of Panax ginseng. Ginsenoside Re is one of the major ginsenosides; whereas hydrolysis products such as Rd appear to have higher biological activity though are present in smaller amounts. Ginsenosides, from their early use in folk medicine to modern studies, appear to exert beneficial actions against aging and even neurodegenerative disorders. Parkinson's disease is a progressive neurodegenerative movement disorder characterized by a profound loss of midbrain dopamine neurons in the substantia nigra pars compacta. Carbon tetrachloride (CCl4) exerts neurotoxic effects when present as an environmental pollutant. As a model compound it was used here to study the impact on primary nigrostriatal dopaminergic nerve cells and to investigate the neuroprotective potential of ginsenosides Rd and Re against this organic solvent. CCl4 (2.5 mM on day 12 in vitro for 48 h) significantly decreased the number of tyrosine hydroxylase (TH+) cells by 51% compared with untreated control cultures, reduced their neuritic lengths, and led to truncated degenerations of cell morphology. Ginsenosides Rd and Re (10 µM) strongly reduced cell loss and degeneration and significantly protected process lengths and numbers of neurites of TH+ cells. The anti-oxidative and anti-inflammatory potential of the cellular supernatant was lowered by CCl4 exposure. Inclusion of ginsenosides inhibited both oxidative stress and inflammation. Therefore the neuroprotective effects of ginsenosides at least partially depend on lowering oxidative stress and anti-inflammation.

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人参皂苷Rd和人参皂苷Re在帕金森病的新模型中提供神经保护。
人参皂苷是人参的主要活性成分。人参皂苷Re是主要的人参皂苷之一;而像Rd这样的水解产物虽然数量较少,但似乎具有更高的生物活性。从民间医学的早期使用到现代研究,人参皂苷似乎对衰老甚至神经退行性疾病都有有益的作用。帕金森病是一种进行性神经退行性运动障碍,其特征是黑质致密部中脑多巴胺神经元的严重丧失。四氯化碳(CCl4)作为一种环境污染物存在时具有神经毒性作用。作为模型化合物,本文研究了人参皂苷Rd和Re对原代黑质纹状体多巴胺能神经细胞的影响,并研究了人参皂苷Rd和Re对该有机溶剂的神经保护作用。CCl4 (2.5 mM,第12天体外培养48 h)使酪氨酸羟化酶(TH+)细胞数量比未处理的对照培养减少51%,神经鞘长度减少,细胞形态变性缩短。人参皂苷Rd和Re(10µM)显著降低TH+细胞的细胞丢失和变性,并显著保护TH+细胞的过程长度和神经突数量。CCl4暴露降低了细胞上清液的抗氧化和抗炎潜能。人参皂苷抑制氧化应激和炎症。因此,人参皂苷的神经保护作用至少部分取决于降低氧化应激和抗炎症。
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