Neuroprotective Effect of Curcuminoids Against Inflammation-Mediated Dopaminergic Neurodegeneration in the MPTP Model of Parkinson’s Disease

2012 ◽  
Vol 7 (3) ◽  
pp. 609-618 ◽  
Author(s):  
Rudra P. Ojha ◽  
Manisha Rastogi ◽  
B. Parimala Devi ◽  
Aruna Agrawal ◽  
G. P. Dubey
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuroprotective Effect ◽  
Dopaminergic Neurodegeneration ◽  
Mptp Model

scholarly journals TFE3-Mediated Autophagy is Involved in Dopaminergic Neurodegeneration in Parkinson’s Disease

2021 ◽  
Vol 9 ◽  
Author(s):  
Xin He ◽  
Yue Xie ◽  
Qiongping Zheng ◽  
Zeyu Zhang ◽  
Shanshan Ma ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Transcription Factor ◽  
Dopaminergic Neurons ◽  
Essential Role ◽  
Dopaminergic Neurodegeneration ◽  
Promising Strategy ◽  
Progressive Loss ◽  
Mptp Model

Impairment of autophagy has been strongly implicated in the progressive loss of nigral dopaminergic neurons in Parkinson’s disease (PD). Transcription factor E3 (TFE3), an MiTF/TFE family transcription factor, has been identified as a master regulator of the genes that are associated with lysosomal biogenesis and autophagy. However, whether TFE3 is involved in parkinsonian neurodegeneration remains to be determined. In this study, we found decreased TFE3 expression in the nuclei of the dopaminergic neurons of postmortem human PD brains. Next, we demonstrated that TFE3 knockdown led to autophagy dysfunction and neurodegeneration of dopaminergic neurons in mice, implying that reduction of nuclear TFE3 may contribute to autophagy dysfunction-mediated cell death in PD. Further, we showed that enhancement of autophagy by TFE3 overexpression dramatically reversed autophagy downregulation and dopaminergic neurons loss in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD. Taken together, these findings demonstrate that TFE3 plays an essential role in maintaining autophagy and the survival of dopaminergic neurons, suggesting TFE3 activation may serve as a promising strategy for PD therapy.

scholarly journals MOLECULAR MARKERS OF ENDOGENOUS NEUROPROTECTION IN THE BRAIN OF RATS WITH EXPERIMENTAL PARKINSON'S DISEASE AND ON THE BACKGROUND OF USING NEW PHARMACOTHERAPY SCHEMES

2020 ◽  
pp. 31-33
Author(s):  
Volodymyr Maramukha
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Passive Control ◽  
Neuroprotective Effect ◽  
Combined Therapy ◽  
The Elderly ◽  
Dopaminergic Neurodegeneration ◽  
Treatment Regimens ◽  
Neuroprotective Therapy ◽  
Neuroprotective Treatment

Parkinson's disease (PD) is one of the most common neurodegenerative diseases in the elderly. The aim of the study. To study apoptotic processes and their role in the formation of dopaminergic neurodegeneration and to develop new treatment regimens with a specific neuroprotective effect on the dopaminergic system. Materials and methods. The study was carried out on 90 Wistar rats at the age of 6 months weighing 220–290 grams. Parkinsonism was induced by the administration of the neurotoxin MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) to experimental rats with neuroprotective treatment: I – Intact (passive control); II – animals with experimental Parkinson's disease (PD, active control); III – PD + Amantadine (AM) IV – PD + AM + Cerebrocurin; V – PD + AM + Pramistar; VI – PD + AM + Gliatilin; VII – PD + AM + Noofen; VIII – PD + AM + Pronoran; IX – PD + AM + Melatonin. Results. The obtained data indicate that neuroprotective therapy of PD with drugs such as melatonin, cerebrocurin, pronoran and gliatilin in combination with amantadine leads to an increase in the expression of the HIF-1α, HIF-3α, HSP70 genes, bcl-2 proteins and decrease c-fos proteins with caspase-3 as markers of apoptosis and can also serve as a molecular marker for the activation of endogenous neuroprotection mechanisms under the conditions of an experimental PD. Conclusions. The study experimentally demonstrated a new target of neuroprotection in PD conditions – apoptosis of dopamine-producing neurons and substantiated modulators of this process – drugs for combined therapy with amantadine (melatonin, cerebrocurin, pronoran and gliatilin) ​​as promising drugs for the treatment of PD.

The Neuroprotective Effect of Fisetin in the MPTP Model of Parkinson's Disease

2012 ◽  
Vol 2 (4) ◽  
pp. 287-302 ◽  
Author(s):  
Mital Y. Patel ◽  
Hirenkumar V. Panchal ◽  
Othman Ghribi ◽  
Kenza E. Benzeroual
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuroprotective Effect ◽  
Mptp Model

scholarly journals Fisetin Regulates Gut Microbiota and Exerts Neuroprotective Effect on Mouse Model of Parkinson’s Disease

2020 ◽  
Vol 14 ◽  
Author(s):  
Tian-Jiao Chen ◽  
Ya Feng ◽  
Te Liu ◽  
Ting-Ting Wu ◽  
Ya-Jing Chen ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Gut Microbiota ◽  
Neuroprotective Effect ◽  
Mice Model ◽  
Alpha And Beta Diversity ◽  
Dopaminergic Neurodegeneration ◽  
Anti Cancer ◽  
Fresh Feces ◽  
Anti Oxidant

Previous studies have reported the anti-oxidant, anti-inflammatory, and anti-cancer effects of fisetin. However, the therapeutic efficacy of fisetin in Parkinson’s disease (PD) is unclear. In this study, we demonstrated that fisetin could markedly alleviate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurodegeneration in mice. To confirm the reported correlation between gut microbiota and PD, the bacterial DNA in the fresh feces of mice from each group was subjected to 16S rRNA (V3 and V4 regions) sequencing. The results revealed that fisetin changed the number, diversity, and distribution of gut microbiota in MPTP-induced mice model of PD. The alpha and beta diversity analyses showed that the fisetin intervented MPTP group gut microbiota exhibited a significantly higher abundance of Lachnospiraceae and a significantly lower abundance of uncultured_bacterium_g_Escherichia-Shigella and uncultured_bacterium_g_Bacillus than the MPTP group gut microbiota. These findings indicated that fisetin exerts a neuroprotective effect on neurodegeneration by altering the composition and diversity of gut microbiota. Thus, fisetin could be a potential novel therapeutic for PD.

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