Rosmarinic acid protects against MPTP-induced toxicity and inhibits iron-induced α-synuclein aggregation

Qu, Le; Xu, Huamin; Jia, Wenting; Jiang, Hong; Xie, Junxia

doi:10.1016/j.neuropharm.2018.09.042

Cited by 38 publications

(16 citation statements)

References 48 publications

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“…Long-term exposure of cells or tissues to OS or excessive ROS can lead to cellular and tissue damage. In accordance with previous reports 46 , our present study revealed that Fen significantly upregulated ROS levels and HO-1 expression and reduced both the expression of SOD-1 and the enzymatic activity of total SOD-1 in primary neurons. Correspondingly, the expression of SOD-1 was also significantly decreased, whereas oxidative proteins and lipids were increased, in the SNpc of striatal Fen-treated mice.…”

Section: Discussionsupporting

confidence: 93%

Fenpropathrin induces degeneration of dopaminergic neurons via disruption of the mitochondrial quality control system

Jiao

2020

Cell Death Discov.

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The synthetic pyrethroid derivative, fenpropathrin, is a widely used insecticide. However, a variety of toxic effects in mammals have been reported. In particular, fenpropathrin induces degeneration of dopaminergic neurons and parkinsonism. However, the mechanism of fenpropathrin-induced parkinsonism has remained unknown. In the present study, we investigated the toxic effects and underlying mechanisms of fenpropathrin on perturbing the dopaminergic system both in vivo and in vitro. We found that fenpropathrin induced cellular death of dopaminergic neurons in vivo. Furthermore, fenpropathrin increased the generation of reactive oxygen species, disrupted both mitochondrial function and dynamic networks, impaired synaptic communication, and promoted mitophagy in vitro. In mice, fenpropathrin was administered into the striatum via stereotaxic (ST) injections. ST-injected mice exhibited poor locomotor function at 24 weeks after the first ST injection and the number of tyrosine hydroxylase (TH)-positive cells and level of TH protein in the substantia nigra pars compacta were significantly decreased, as compared to these parameters in vehicle-treated mice. Taken together, our results demonstrate that exposure to fenpropathrin induces a loss of dopaminergic neurons and partially mimics the pathologic features of Parkinson's disease. These findings suggest that fenpropathrin may induce neuronal degeneration via dysregulation of mitochondrial function and the mitochondrial quality control system.

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Section: Discussionsupporting

confidence: 93%

Fenpropathrin induces degeneration of dopaminergic neurons via disruption of the mitochondrial quality control system

Jiao

2020

Cell Death Discov.

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“… 23 , 24 , 25 , 26 , 27 Meanwhile, there are several reports that explored protein aggregation and neuro-inflammation using the models induced by MPTP. 25 , 28 , 29 , 30 , 31 Furthermore, HOTAIR downregulation was found to enhance cell apoptosis of dopaminergic neurons in the substantia nigra pars compacta. Correspondingly, HOTAIR has been found to be overexpressed in a variety of human cancers and diseases and is believed to trigger cancer occurrence and progression by regulating cell invasion and apoptosis.…”

Section: Discussionmentioning

confidence: 95%

RETRACTED: HOTAIR Accelerates Dyskinesia in a MPTP-Lesioned Mouse Model of PD via SSTR1 Methylation-Mediated ERK1/2 Axis

Cai

Yang

et al. 2020

Molecular Therapy - Nucleic Acids

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Homeobox transcript antisense RNA (HOTAIR), has been associated with neuroprotective effects in Parkinson’s disease (PD). However, the underlying mechanisms still remain unclear. Hence, this present study attempted to clarify the functional relevance of HOTAIR in PD. We established an in vivo mouse model of PD using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and an in vitro cell model of PD by treating dopaminergic neuron MN9D cells with 1-methyl-4-phenylpyridinium species (MPP + ). The expressions of somatostatin receptor 1 (SSTR1) and HOTAIR were altered to examine their effects on MN9D cell viability and apoptosis, as well as on movement impairments in MPTP-induced PD mouse model. The results indicated that HOTAIR expression was upregulated and SSTR1 was downregulated in in vivo and in vitro PD models. HOTAIR could bind to the promoter region of SSTR1, resulting in an increase of SSTR1 methylation through the recruitment of DNA methyltransferases in PD cell models. Notably, overexpression of HOTAIR and silencing of SSTR1 enhanced dopaminergic neuron apoptosis in MN9D cells and exacerbated dyskinesia in MPTP-induced PD mouse model. Collectively, overexpressed HOTAIR stimulates DNA methylation of SSTR1 to reduce SSTR1 expression, thereby accelerating dyskinesia and facilitating dopaminergic neuron apoptosis in a MPTP-lesioned PD mouse model via activation of the ERK1/2 axis.

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“…Curcumin is a well-known antioxidant that can increase the solubility of the α-synuclein form of monomers in catecholaminergic cell lines and in vivo models, thereby inhibiting oligomerization [168,169,170,171]. Pretreatment of rosmarinic acid inhibits reduction in the mitochondrial membrane potential and α-synuclein aggregation through its iron-chelating activity in an MPTP-induced PD model [110]. In addition, myricetin can inhibit α-synuclein oligomerization by directly binding to the α-synuclein N-terminal region in vitro [90].…”

Section: Natural Compounds Ameliorating Proteostasis Impairment In Pdmentioning

confidence: 99%

Amelioration of Mitochondrial Quality Control and Proteostasis by Natural Compounds in Parkinson’s Disease Models

Cho

Kim

Huh

et al. 2019

IJMS

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Parkinson’s disease (PD) is a well-known age-related neurodegenerative disorder associated with longer lifespans and rapidly aging populations. The pathophysiological mechanism is a complex progress involving cellular damage such as mitochondrial dysfunction and protein homeostasis. Age-mediated degenerative neurological disorders can reduce the quality of life and also impose economic burdens. Currently, the common treatment is replacement with levodopa to address low dopamine levels; however, this does not halt the progression of PD and is associated with adverse effects, including dyskinesis. In addition, elderly patients can react negatively to treatment with synthetic neuroprotection agents. Recently, natural compounds such as phytochemicals with fewer side effects have been reported as candidate treatments of age-related neurodegenerative diseases. This review focuses on mitochondrial dysfunction, oxidative stress, hormesis, proteostasis, the ubiquitin‒proteasome system, and autophagy (mitophagy) to explain the neuroprotective effects of using natural products as a therapeutic strategy. We also summarize the efforts to use natural extracts to develop novel pharmacological candidates for treatment of age-related PD.

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Rosmarinic acid protects against MPTP-induced toxicity and inhibits iron-induced α-synuclein aggregation

Cited by 38 publications

References 48 publications

Fenpropathrin induces degeneration of dopaminergic neurons via disruption of the mitochondrial quality control system

Fenpropathrin induces degeneration of dopaminergic neurons via disruption of the mitochondrial quality control system

RETRACTED: HOTAIR Accelerates Dyskinesia in a MPTP-Lesioned Mouse Model of PD via SSTR1 Methylation-Mediated ERK1/2 Axis

Amelioration of Mitochondrial Quality Control and Proteostasis by Natural Compounds in Parkinson’s Disease Models

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