Neurogrit Gold Attenuates 6-OHDA-Induced Dopaminergic Neurodegeneration in Parkinson's Model of Caenorhabditis elegans by Reducing α-Synuclein Accumulation and Pink/Pdr-1 Driven Mitochondrial Dysfunction

IF 4.8 1区 医学 Q1 NEUROSCIENCES
Acharya Balkrishna, Nishit Pathak, Rani Singh, Vivek Gohel, Yash Varshney, Rishabh Dev, Anurag Varshney
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引用次数: 0

Abstract

Introduction

Parkinson's disease (PD) is a neurodegenerative disorder majorly associated with movement and behavioral disturbances. Pathologically, the loss of dopaminergic (DA) neurons triggered by the deposition of α-synuclein (SNCA) leads to the decrease in dopamine levels affecting motor and cognitive functions of the brain. Current pharmacotherapy for PD only addresses its symptoms but is not able to halt its progression. Traditional medicines are being increasingly used for the treatment of neurodegenerative disorders.

Aim

The present study investigated the effects of Neurogrit Gold (NG), a herbo-mineral prescription medicine, on a Parkinson's model of Caenorhabditis elegans.

Methods

Chemical characterization of NG was performed on HPLC and GC–MS/MS platforms. Evaluation of NG was done in the neurotoxicant 6-OHDA-induced N2, BZ555, and NL5901 strains of C. elegans.

Results

It was observed that NG treatment did not hamper the lifespan, survival, and progeny development of C. elegans strains. The worms treated with NG were able to resist the deleterious effects of 6-OHDA on survival, progeny development, body bends, and chemotaxis in N2 and DA neuron degeneration in BZ555 worms. In NL5901 worms, NG treatment reduced SNCA aggregation, restored lipid content, as well as improved body bends, chemotaxis, and food uptake. Gene expression studies on 6-OHDA exposed and NG-treated N2 worms suggest that the neuroprotective effects of NG stem from its ability to regulate genes involved in mitochondrial autophagy (pink-1, pdr-1); dopamine synthesis (cat-2); redox (sod-3) and protein folding homeostasis (hsf-1, hsp-12.3).

Conclusion

Neurogrit Gold has robust neuroprotective effects, making it a suitable treatment option against etiologies of Parkinson's disease.

Abstract Image

神经砂金通过减少α-突触核蛋白积累和粉红色/Pdr-1驱动的线粒体功能障碍,减轻6-羟色胺诱导的秀丽隐杆线虫帕金森模型中多巴胺能神经退行性变
帕金森病(PD)是一种主要与运动和行为障碍相关的神经退行性疾病。病理上,α-突触核蛋白(SNCA)沉积引发多巴胺能(DA)神经元的丧失,导致多巴胺水平下降,影响大脑的运动和认知功能。目前PD的药物治疗仅针对其症状,但不能阻止其进展。传统药物越来越多地用于治疗神经退行性疾病。目的观察神经砂金(NG)对秀丽隐杆线虫帕金森病模型的影响。方法采用高效液相色谱(HPLC)和气相色谱-质谱(GC-MS /MS)对NG进行化学表征。对神经毒性6- ohda诱导的秀丽隐杆线虫N2、BZ555和NL5901株进行了NG的评价。结果NG处理对秀丽隐杆线虫的寿命、存活和后代发育无明显影响。NG处理的线虫能够抵抗6-OHDA对BZ555线虫存活、后代发育、体弯曲、N2趋化性和DA神经元退化的有害影响。在NL5901蠕虫中,NG处理降低了SNCA聚集,恢复了脂质含量,并改善了体弯曲、趋化性和食物摄取。对6-OHDA暴露和NG处理的N2蠕虫的基因表达研究表明,NG的神经保护作用源于其调节线粒体自噬相关基因的能力(粉色-1,pdr-1);多巴胺合成(cat-2);氧化还原(sod-3)和蛋白质折叠稳态(hsf-1, hsp-12.3)。结论神经砂金具有较强的神经保护作用,是治疗帕金森病病因的理想选择。
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来源期刊
CNS Neuroscience & Therapeutics
CNS Neuroscience & Therapeutics 医学-神经科学
CiteScore
7.30
自引率
12.70%
发文量
240
审稿时长
2 months
期刊介绍: CNS Neuroscience & Therapeutics provides a medium for rapid publication of original clinical, experimental, and translational research papers, timely reviews and reports of novel findings of therapeutic relevance to the central nervous system, as well as papers related to clinical pharmacology, drug development and novel methodologies for drug evaluation. The journal focuses on neurological and psychiatric diseases such as stroke, Parkinson’s disease, Alzheimer’s disease, depression, schizophrenia, epilepsy, and drug abuse.
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