The Neuroprotective Role of MiR-124-3p in a 6-Hydroxydopamine-Induced Cell Model of Parkinson's Disease via the Regulation of ANAX5

2017 ◽  
Vol 119 (1) ◽  
pp. 269-277 ◽  
Author(s):  
Rui-Fang Dong ◽  
Bing Zhang ◽  
Li-Wen Tai ◽  
Hong-Mei Liu ◽  
Fang-Kun Shi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Model ◽  
6 Hydroxydopamine

scholarly journals The Protective Role of Brain CYP2J in Parkinson’s Disease Models

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Yueran Li ◽  
Jinhua Wu ◽  
Xuming Yu ◽  
Shufang Na ◽  
Ke Li ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Brain Regions ◽  
Protective Role ◽  
Neural Cells ◽  
Endogenous Substrates ◽  
6 Hydroxydopamine ◽  
Myd88 Signaling ◽  
Lps Treatment

CYP2J proteins are present in the neural cells of human and rodent brain regions. The aim of this study was to investigate the role of brain CYP2J in Parkinson’s disease. Rats received right unilateral injection with lipopolysaccharide (LPS) or 6-hydroxydopamine (6-OHDA) in the substantia nigra following transfection with or without the CYP2J3 expression vector. Compared with LPS-treated rats, CYP2J3 transfection significantly decreased apomorphine-induced rotation by 57.3% at day 12 and 47.0% at day 21 after LPS treatment; moreover, CYP2J3 transfection attenuated the accumulation of α-synuclein. Compared with the 6-OHDA group, the number of rotations by rats transfected with CYP2J3 decreased by 59.6% at day 12 and 43.5% at day 21 after 6-OHDA treatment. The loss of dopaminergic neurons and the inhibition of the antioxidative system induced by LPS or 6-OHDA were attenuated following CYP2J3 transfection. The TLR4-MyD88 signaling pathway was involved in the downregulation of brain CYP2J induced by LPS, and CYP2J transfection upregulated the expression of Nrf2 via the inhibition of miR-340 in U251 cells. The data suggest that increased levels of CYP2J in the brain can delay the pathological progression of PD initiated by inflammation or neurotoxins. The alteration of the metabolism of the endogenous substrates (e.g., AA) could affect the risk of neurodegenerative disease.

scholarly journals Lipid Analysis of the 6-Hydroxydopamine-Treated SH-SY5Y Cell Model for Parkinson’s Disease

2019 ◽  
Vol 57 (2) ◽  
pp. 848-859 ◽  
Author(s):  
Helena Xicoy ◽  
Jos F. Brouwers ◽  
Oleksandra Kalnytska ◽  
Bé Wieringa ◽  
Gerard J. M. Martens
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Lipid Analysis ◽  
Cell Model ◽  
6 Hydroxydopamine

Protective role of chrysin on 6-hydroxydopamine-induced neurodegeneration a mouse model of Parkinson's disease: Involvement of neuroinflammation and neurotrophins

2018 ◽  
Vol 279 ◽  
pp. 111-120 ◽  
Author(s):  
André T.R. Goes ◽  
Cristiano R. Jesse ◽  
Michelle S. Antunes ◽  
Fernando V. Lobo Ladd ◽  
Aliny A.B. Lobo Ladd ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Protective Role ◽  
6 Hydroxydopamine

scholarly journals The Role of NOX4 in Parkinson’s Disease with Dementia

2019 ◽  
Vol 20 (3) ◽  
pp. 696 ◽  
Author(s):  
Dong-Hee Choi ◽  
In-Ae Choi ◽  
Cheol Lee ◽  
Ji Yun ◽  
Jongmin Lee
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Impairment ◽  
Alpha Synuclein ◽  
Cognitive Status ◽  
Dopamine Neurons ◽  
Parkinson’S Disease With Dementia ◽  
6 Hydroxydopamine ◽  
Nigrostriatal Dopamine Neurons

The neuropathology of Parkinson’s disease with dementia (PDD) has been reported to involve heterogeneous and various disease mechanisms. Alpha-synuclein (α-syn) and amyloid beta (Aβ) pathology are associated with the cognitive status of PDD, and NADPH oxidase (NOX) is known to affect a variety of cognitive functions. We investigated the effects of NOX on cognitive impairment and on α-syn and Aβ expression and aggregation in PDD. In the 6-hydroxydopamine (6-OHDA)-injected mouse model, cognitive and motor function, and the levels of α-syn, Aβ, and oligomer A11 after inhibition of NOX4 expression in the hippocampal dentate gyrus (DG) were measured by the Morris water maze, novel object recognition, rotation, and rotarod tests, as well as immunoblotting and immunohistochemistry. After 6-OHDA administration, the death of nigrostriatal dopamine neurons and the expression of α-syn and NOX1 in the substantia nigra were increased, and phosphorylated α-syn, Aβ, oligomer A11, and NOX4 were upregulated in the hippocampus. 6-OHDA dose-dependent cognitive impairment was observed, and the increased cognitive impairment, Aβ expression, and oligomer A11 production in 6-OHDA-treated mice were suppressed by NOX4 knockdown in the hippocampal DG. Our results suggest that increased expression of NOX4 in the hippocampal DG in the 6-OHDA-treated mouse induces Aβ expression and oligomer A11 production, thereby reducing cognitive function.

scholarly journals Therapeutic Effects of Fucoidan in 6-Hydroxydopamine-Lesioned Rat Model of Parkinson's disease: Role of NADPH oxidase-1

2014 ◽  
Vol 20 (12) ◽  
pp. 1036-1044 ◽  
Author(s):  
Fei-Long Zhang ◽  
Yi He ◽  
Yan Zheng ◽  
Wen-Jing Zhang ◽  
Qi Wang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nadph Oxidase ◽  
Rat Model ◽  
Therapeutic Effects ◽  
Nadph Oxidase 1 ◽  
6 Hydroxydopamine

scholarly journals Neural Repair Strategies for Parkinson's Disease: Insights from Primate Models

2006 ◽  
Vol 15 (3) ◽  
pp. 251-265 ◽  
Author(s):  
Katherine Soderstrom ◽  
Jennifer O'malley ◽  
Kathy Steece-Collier ◽  
Jeffrey H. Kordower
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nonhuman Primate ◽  
Trophic Factor ◽  
Novel Therapies ◽  
Neural Repair ◽  
Advantages And Disadvantages ◽  
6 Hydroxydopamine ◽  
Deep Brain

Nonhuman primate models of Parkinson's disease (PD) have been invaluable to our understanding of the human disease and in the advancement of novel therapies for its treatment. In this review, we attempt to give a brief overview of the animal models of PD currently used, with a more comprehensive focus on the advantages and disadvantages presented by their use in the nonhuman primate. In particular, discussion addresses the 6-hydroxydopamine (6-OHDA), 1-methyl-1,2,3,6-tetrahydopyridine (MPTP), rotenone, paraquat, and maneb parkinsonian models. Additionally, the role of primate PD models in the development of novel therapies, such as trophic factor delivery, grafting, and deep brain stimulation, are described. Finally, the contribution of primate PD models to our understanding of the etiology and pathology of human PD is discussed.

scholarly journals Anti-Apoptotic and Anti-Inflammatory Role of Trans ε-Viniferin in a Neuron–Glia Co-Culture Cellular Model of Parkinson’s Disease

Foods ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 586
Author(s):  
Domenico Sergi ◽  
Alex Gélinas ◽  
Jimmy Beaulieu ◽  
Justine Renaud ◽  
Emilie Tardif-Pellerin ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nerve Growth Factor ◽  
Culture System ◽  
Cellular Model ◽  
Dopaminergic Cells ◽  
Inflammatory Molecule ◽  
Anti Inflammatory ◽  
6 Hydroxydopamine

The polyphenol trans-ε-viniferin (viniferin) is a dimer of resveratrol, reported to hold antioxidant and anti-inflammatory properties. The aims of our study were to evaluate the neuroprotective potential of viniferin in the nerve growth factor (NGF)-differentiated PC12 cells, a dopaminergic cellular model of Parkinson’s disease (PD) and assess its anti-inflammatory properties in a N9 microglia–neuronal PC12 cell co-culture system. The neuronal cells were pre-treated with viniferin, resveratrol or their mixture before the administration of 6-hydroxydopamine (6-OHDA), recognized to induce parkinsonism in rats. Furthermore, N9 microglia cells, in a co-culture system with neuronal PC12, were pre-treated with viniferin, resveratrol or their mixture to investigate whether these polyphenols could reduce lipopolysaccharide (LPS)-induced inflammation. Our results show that viniferin as well as a mixture of viniferin and resveratrol protects neuronal dopaminergic cells from 6-OHDA-induced cytotoxicity and apoptosis. Furthermore, when viniferin, resveratrol or their mixture was used to pre-treat microglia cells in our co-culture system, they reduced neuronal cytotoxicity induced by glial activation. Altogether, our data highlight a novel role for viniferin as a neuroprotective and anti-inflammatory molecule in a dopaminergic cellular model, paving the way for nutraceutical therapeutic avenues in the complementary treatments of PD.

scholarly journals Chaperone Sigma1R mediates the neuroprotective action of afobazole in the 6-OHDA model of Parkinson’s disease

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mikhail V. Voronin ◽  
Ilya A. Kadnikov ◽  
Dmitry N. Voronkov ◽  
Sergey B. Seredenin
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuroprotective Effect ◽  
Treatment Options ◽  
Striatal Dopamine ◽  
Dopamine Content ◽  
Sigma 1 ◽  
6 Hydroxydopamine ◽  
Therapeutic Perspective

AbstractParkinson’s disease (PD) is a progressive neurodegenerative disease with limited treatment options. Therefore, the identification of therapeutic targets is urgently needed. Previous studies have shown that the ligand activation of the sigma-1 chaperone (Sigma1R) promotes neuroprotection. The multitarget drug afobazole (5-ethoxy-2-[2-(morpholino)-ethylthio]benzimidazole dihydrochloride) was shown to interact with Sigma1Rs and prevent decreases in striatal dopamine in the 6-hydroxydopamine (6-OHDA)-induced parkinsonism model. The aim of the present study was to elucidate the role of Sigma1Rs in afobazole pharmacological activity. Using ICR mice we found that administration of afobazole (2.5 mg/kg, i.p.) or selective agonist of Sigma1R PRE-084 (1.0 mg/kg, i.p.) over 14 days normalizes motor disfunction and prevents decreases in dopamine in the 6-OHDA-lesioned striatum. Afobazole administration also prevents the loss of TH + neurons in the substantia nigra. The pre-administration of selective Sigma1R antagonist BD-1047 (3.0 mg/kg, i.p.) abolishes the activity of either afobazole or PRE-084, as determined using the rotarod test and the analysis of striatal dopamine content. The current study demonstrates the contribution of Sigma1Rs in the neuroprotective effect of afobazole in the 6-OHDA model of Parkinson’s disease and defines the therapeutic perspective of Sigma1R agonists in the clinic.

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