scholarly journals Inhibition of Tau Phosphorylation as a Potential Strategy in Treatment of Parkinson’s Disease

Author(s):  
Wang Wenya
2020 ◽  
Vol 13 ◽  
Author(s):  
Zhang Mao ◽  
Zhu Wen-ting ◽  
Wang Hai-tao ◽  
Yu Hui ◽  
Lan Shi-yi ◽  
...  

2014 ◽  
Author(s):  
Mojtaba Golpich ◽  
Behrouz Rahmani ◽  
Norlinah Mohamed Ibrahim ◽  
Leila Dargahi ◽  
Zahurin Mohamed ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-9
Author(s):  
Yihui Xu ◽  
Wei Lin ◽  
Shuifen Ye ◽  
Huajin Wang ◽  
Tingting Wang ◽  
...  

Oxidative damage plays a critical role in the etiology of neurodegenerative disorders including Parkinson’s disease (PD). In our study, an ancient Chinese kidney-tonifying formula, which consists ofCistanche,Epimedii,andPolygonatum cirrhifolium, was investigated to protect MES23.5 dopaminergic neurons against hydrogen peroxide- (H2O2-) induced oxidative damage. The damage effects of H2O2on MES23.5 cells and the protective effects of KTF against oxidative stress were evaluated using MTT assay, transmission electron microscopy (TEM), immunocytochemistry (ICC), enzyme-linked immunosorbent assay (ELISA), and immunoblotting. The results showed that cell viability was dramatically decreased after a 12 h exposure to 150 μM H2O2. TEM observation found that the H2O2-treated MES23.5 cells presented cellular organelle damage. However, when cells were incubated with KTF (3.125, 6.25, and 12.5 μg/ml) for 24 h after H2O2exposure, a significant protective effect against H2O2-induced damage was observed in MES23.5 cells. Using ICC, we found that KTF inhibited the reduction of the tyrosine hydroxylase (TH) induced by H2O2, upregulated the mRNA and protein expression of HO-1, CAT, and GPx-1, and downregulated the expression of caspase 3. These results indicated that KTF may provide neuron protection against H2O2-induced cell damage through ameliorating oxidative stress, and our findings provide a new potential strategy for the prevention and treatment of Parkinson’s disease.


2014 ◽  
Vol 51 (1) ◽  
pp. 313-330 ◽  
Author(s):  
Mojtaba Golpich ◽  
Behrouz Rahmani ◽  
Norlinah Mohamed Ibrahim ◽  
Leila Dargahi ◽  
Zahurin Mohamed ◽  
...  

ChemMedChem ◽  
2006 ◽  
Vol 1 (2) ◽  
pp. 256-266 ◽  
Author(s):  
Alan P. Kozikowski ◽  
Irina N. Gaisina ◽  
Pavel A. Petukhov ◽  
Jayalakshmi Sridhar ◽  
LaShaunda T. King ◽  
...  

2009 ◽  
Vol 23 (9) ◽  
pp. 2820-2830 ◽  
Author(s):  
Tetyana Duka ◽  
Valeriy Duka ◽  
Jeffrey N. Joyce ◽  
Anita Sidhu

2021 ◽  
Vol 22 (3) ◽  
pp. 1324
Author(s):  
Jun Ho Lee ◽  
Hong Jun Kim ◽  
Jong Uk Kim ◽  
Tae Han Yook ◽  
Kyeong Han Kim ◽  
...  

Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most common neurodegenerative diseases. Many studies have demonstrated that the release of NLRP3 inflammasome-mediated proinflammatory cytokines by the excessive activation of microglia is associated with the pathogenesis of AD and PD and suggested that the NLRP3 inflammasome plays an important role in AD and PD development. In both diseases, various stimuli, such as Aβ and α-synuclein, accelerate the formation of the NLRP3 inflammasome in microglia and induce pyroptosis through the expression of interleukin (IL)-1β, caspase-1, etc., where neuroinflammation contributes to gradual progression and deterioration. However, despite intensive research, the exact function and regulation of the NLRP3 inflammasome has not yet been clearly identified. Moreover, there have not yet been any experiments of clinical use, although many studies have recently been conducted to improve treatment of inflammatory diseases using various inhibitors for NLRP3 inflammasome pathways. However, recent studies have reported that various natural products show improvement effects in the in vivo models of AD and PD through the regulation of NLRP3 inflammasome assembly. Therefore, the present review provides an overview of natural extraction studies aimed at the prevention or treatment of NLRP3 inflammasome-mediated neurological disorders. It is suggested that the discovery and development of these various natural products could be a potential strategy for NLRP3 inflammasome-mediated AD and PD treatment.


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