Silibinin prevents dopaminergic neuronal loss in a mouse model of Parkinson's disease via mitochondrial stabilization

2015 ◽  
Vol 93 (5) ◽  
pp. 755-765 ◽  
Author(s):  
Yujeong Lee ◽  
Hee Ra Park ◽  
Hye Jeong Chun ◽  
Jaewon Lee
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Neuronal Loss ◽  
Dopaminergic Neuronal Loss

scholarly journals MMP-3 Contributes to Nigrostriatal Dopaminergic Neuronal Loss, BBB Damage, and Neuroinflammation in an MPTP Mouse Model of Parkinson’s Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Young Cheul Chung ◽  
Yoon-Seong Kim ◽  
Eugene Bok ◽  
Tae Young Yune ◽  
Sungho Maeng ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Neuroprotective Effect ◽  
Neuronal Loss ◽  
Nigrostriatal Pathway ◽  
Matrix Metalloproteinase 3 ◽  
Genetic Ablation ◽  
Dopaminergic Neuronal Loss ◽  
Peripheral Immune Cells

The present study examined whether matrix metalloproteinase-3 (MMP-3) participates in the loss of dopaminergic (DA) neurons in the nigrostriatal pathway in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease with blood brain barrier (BBB) damage and infiltration of peripheral immune cells. Tyrosine hydroxylase (TH) immunostaining of brain sections from MPTP-treated mice showed that MPTP induced significant degeneration of nigrostriatal DA neurons. Moreover, FITC-labeled albumin detection and immunostaining revealed that MPTP caused damage to the BBB and increased the number of ED-1- and CD-3-immunopositive cells in the substantia nigra (SN). Genetic ablation of MMP-3 reduced the nigrostriatal DA neuron loss and improved motor function. This neuroprotective effect afforded by MMP-3 deletion was associated with the suppression of BBB disruption and a decrease in the number of ED-1- and CD-3-immunopositive cells in the SN. These data suggest that MMP-3 could play a crucial role in neurodegenerative diseases such as PD in which BBB damage and neuroinflammation are implicated.

scholarly journals Hydrogen in Drinking Water Reduces Dopaminergic Neuronal Loss in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine Mouse Model of Parkinson's Disease

PLoS ONE ◽  
2009 ◽  
Vol 4 (9) ◽  
pp. e7247 ◽  
Author(s):  
Kyota Fujita ◽  
Toshihiro Seike ◽  
Noriko Yutsudo ◽  
Mizuki Ohno ◽  
Hidetaka Yamada ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Drinking Water ◽  
Mouse Model ◽  
Neuronal Loss ◽  
Dopaminergic Neuronal Loss

scholarly journals Selective inhibition of NF- B activation prevents dopaminergic neuronal loss in a mouse model of Parkinson's disease

2007 ◽  
Vol 104 (47) ◽  
pp. 18754-18759 ◽  
Author(s):  
A. Ghosh ◽  
A. Roy ◽  
X. Liu ◽  
J. H. Kordower ◽  
E. J. Mufson ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Neuronal Loss ◽  
Selective Inhibition ◽  
Dopaminergic Neuronal Loss

scholarly journals Gut microbiota-derived propionate mediates the neuroprotective effect of osteocalcin in a mouse model of Parkinson’s disease

Microbiome ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Yan-fang Hou ◽  
Chang Shan ◽  
Si-yue Zhuang ◽  
Qian-qian Zhuang ◽  
Arijit Ghosh ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Gut Microbiota ◽  
Neuronal Loss ◽  
Underlying Mechanism ◽  
Enteric Neurons ◽  
Motor Deficits ◽  
Neuroprotective Effects ◽  
Dopaminergic Neuronal Loss

Abstract Background Parkinson’s disease (PD) is a neurodegenerative disorder with no absolute cure. The evidence of the involvement of gut microbiota in PD pathogenesis suggests the need to identify certain molecule(s) derived from the gut microbiota, which has the potential to manage PD. Osteocalcin (OCN), an osteoblast-secreted protein, has been shown to modulate brain function. Thus, it is of interest to investigate whether OCN could exert protective effect on PD and, if yes, whether the underlying mechanism lies in the subsequent changes in gut microbiota. Results The intraperitoneal injection of OCN can effectively ameliorate the motor deficits and dopaminergic neuronal loss in a 6-hydroxydopamine-induced PD mouse model. The further antibiotics treatment and fecal microbiota transplantation experiments confirmed that the gut microbiota was required for OCN-induced protection in PD mice. OCN elevated Bacteroidetes and depleted Firmicutes phyla in the gut microbiota of PD mice with elevated potential of microbial propionate production and was confirmed by fecal propionate levels. Two months of orally administered propionate successfully rescued motor deficits and dopaminergic neuronal loss in PD mice. Furthermore, AR420626, the agonist of FFAR3, which is the receptor of propionate, mimicked the neuroprotective effects of propionate and the ablation of enteric neurons blocked the prevention of dopaminergic neuronal loss by propionate in PD mice. Conclusions Together, our results demonstrate that OCN ameliorates motor deficits and dopaminergic neuronal loss in PD mice, modulating gut microbiome and increasing propionate level might be an underlying mechanism responsible for the neuroprotective effects of OCN on PD, and the FFAR3, expressed in enteric nervous system, might be the main action site of propionate.

Dopaminergic neuronal loss in transgenic mice expressing the Parkinson's disease-associated UCH-L1 I93M mutant

2007 ◽  
Vol 50 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Rieko Setsuie ◽  
Yu-Lai Wang ◽  
Hideki Mochizuki ◽  
Hitoshi Osaka ◽  
Hideki Hayakawa ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Transgenic Mice ◽  
Neuronal Loss ◽  
Dopaminergic Neuronal Loss
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