Study of molecular mechanism of anti-Parkinson’s disease TraditionalChinese Medicine using model of Caenorhabditis elegans

2010 ◽  
Vol 35 (5) ◽  
Author(s):  
WANG Xiangming
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Caenorhabditis Elegans ◽  
Molecular Mechanism

Potential role of protein stabilizers in amelioration of Parkinson's disease and associated effects in transgenic Caenorhabditis elegans model expressing alpha-synuclein

RSC Advances ◽  
2015 ◽  
Vol 5 (95) ◽  
pp. 77706-77715 ◽  
Author(s):  
Supinder Kaur ◽  
Aamir Nazir
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Caenorhabditis Elegans ◽  
Potential Role ◽  
Alpha Synuclein ◽  
C Elegans

Studies employing transgenicC. elegansmodel show that trehalose, a protein stabilizer, alleviates manifestations associated with Parkinson's diseaseviaits inherent activity and through induction of autophagic machinery.

Dopamine Oxidation Products as Mitochondrial Endotoxins, a Potential Molecular Mechanism for Preferential Neurodegeneration in Parkinson’s Disease

2018 ◽  
Vol 9 (11) ◽  
pp. 2849-2858 ◽  
Author(s):  
Alice Biosa ◽  
Irene Arduini ◽  
Maria Eugenia Soriano ◽  
Valentina Giorgio ◽  
Paolo Bernardi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Molecular Mechanism ◽  
Oxidation Products ◽  
Dopamine Oxidation

scholarly journals Maackiain Ameliorates 6-Hydroxydopamine and SNCA Pathologies by Modulating the PINK1/Parkin Pathway in Models of Parkinson’s Disease in Caenorhabditis elegans and the SH-SY5Y Cell Line

2020 ◽  
Vol 21 (12) ◽  
pp. 4455
Author(s):  
Rong-Tzong Tsai ◽  
Chia-Wen Tsai ◽  
Shih-Ping Liu ◽  
Jia-Xin Gao ◽  
Yun-Hua Kuo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Caenorhabditis Elegans ◽  
Cell Line ◽  
Ubiquitin Proteasome System ◽  
Substantia Nigra Pars Compacta ◽  
Neuron Damage ◽  
6 Hydroxydopamine

The movement disorder Parkinson’s disease (PD) is the second most frequently diagnosed neurodegenerative disease, and is associated with aging, the environment, and genetic factors. The intracellular aggregation of α-synuclein and the loss of dopaminergic neurons in the substantia nigra pars compacta are the pathological hallmark of PD. At present, there is no successful treatment for PD. Maackiain (MK) is a flavonoid extracted from dried roots of Sophora flavescens Aiton. MK has emerged as a novel agent for PD treatment that acts by inhibiting monoamine oxidase B. In this study, we assessed the neuroprotective potential of MK in Caenorhabditis elegans and investigated possible mechanism of this neuroprotection in the human SH-SY5Y cell line. We found that MK significantly reduced dopaminergic neuron damage in 6-hydroxydopamine (6-OHDA)-exposed worms of the BZ555 strain, with corresponding improvements in food-sensing behavior and life-span. In transgenic worms of strain NL5901 treated with 0.25 mM MK, the accumulation of α-synuclein was diminished by 27% (p < 0.01) compared with that in untreated worms. Moreover, in worms and the SH-SY5Y cell line, we confirmed that the mechanism of MK-mediated protection against PD pathology may include blocking apoptosis, enhancing the ubiquitin-proteasome system, and augmenting autophagy by increasing PINK1/parkin expression. The use of small interfering RNA to downregulate parkin expression in vivo and in vitro could reverse the benefits of MK in PD models. MK may have considerable therapeutic applications in PD.

scholarly journals HIGH-MOBILITY GROUP BOX 1 (HMGB1) PROTEIN EVALUATION IN MPTP-INDUCED ZEBRAFISH MODEL OF PARKINSON’S DISEASE

2021 ◽  
Author(s):  
Wael MY Mohamed ◽  
Khairiah Razali ◽  
Noratikah Othman ◽  
Mohamed Hamza ◽  
Abdel Moneem Doolane ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Molecular Mechanism ◽  
High Mobility ◽  
High Mobility Group ◽  
Current Evidence ◽  
Hmgb1 Protein ◽  
Zebrafish Model ◽  
Molecular Studies

Molecular studies have proven beneficial in understanding the pathophysiology of PD. Besides, the advancing application of zebrafish as a PD model has enabled researchers to conduct molecular studies with more promising outcomes and significance. Current evidence reported on the association of HMGB1 protein with neuroinflammation-induced PD pathogenesis. However, to the extent ofour knowledge, the molecular mechanism pertaining to HMGB1 involvement in PD are still elusive. Hence, we propose to conduct a study on HMGB1 protein, to elucidate its role in the pathogenesis of the MPTP-induced zebrafish model of PD. This study will answer the question pertaining to the involvement of HMGB1 in PD development and whether the knockdown of this protein can improve PD symptoms in zebrafish, particularly MPTP-induced motilitydisorders.

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