Therapeutic Effects of Hydrogen in Animal Models of Parkinson's Disease

Fujita, Kyota; Nakabeppu, Yusaku; Нода, Мами

doi:10.4061/2011/307875

Cited by 12 publications

(14 citation statements)

References 89 publications

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“…Thus, we assessed the effects of ginsenoside Re on 6-OHDA-triggered cellular damage by determining the level of lactate dehydrogenase (LDH) released into the medium and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)-based cell viability in SH-SY5Y cells. 6-OHDA significantly increased LDH release into the medium as reported previously [3]. However, this effect was attenuated in the presence of ginsenoside Re ( Figure 3A).…”

Section: Ginsenoside Re Attenuates 6-ohda-triggered Cellular Damagesupporting

confidence: 89%

“…Oxidative stress is implicated in 6-OHDA-triggered cell damage [3]; thus, we examined the effects of ginsenoside Re on the expression of the antioxidant proteins SOD1, GR, CAT, GPX1, and GPX4 in SH-SY5Y cells. Treatment applied induced only changes at the mRNA level of GPX4 ( Figure 4).…”

Section: Ginsenoside Re Upregulates the Expression Of Gpx4mentioning

confidence: 99%

“…6-OHDA easily enters these types of neurons due to its high affinity for both dopaminergic and noradrenergic transporters [2]. Once transported into neurons, 6-OHDA is readily oxidized and this leads to the formation of reactive oxygen species (ROS), which trigger oxidative stress in dopaminergic neurons and ultimately induce cytotoxicity [3]. Thus, 6-OHDA is popularly adopted to generate an animal model of Parkinson's disease (PD)-the progressive neurodegeneration of dopaminergic neurons in the substantia nigra.…”

Section: Introductionmentioning

confidence: 99%

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Ginsenoside Re Mitigates 6-Hydroxydopamine-Induced Oxidative Stress through Upregulation of GPX4

Lee

Hur

et al. 2020

Molecules

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Ginsenosides are active components found abundantly in ginseng which has been used as a medicinal herb to modify disease status for thousands of years. However, the pharmacological activity of ginsenoside Re in the neuronal system remains to be elucidated. Neuroprotective activity of ginsenoside Re was investigated in SH-SY5Y cells exposed to 6-hydroxydopamine (6-OHDA) to induce cellular injury. Ginsenoside Re significantly inhibited 6-OHDA-triggered cellular damage as judged by analysis of tetrazolium dye reduction and lactose dehydrogenase release. In addition, ginsenoside Re induced the expression of the antioxidant protein glutathione peroxidase 4 (GPX4) but not catalase, glutathione peroxidase 1, glutathione reductase, or superoxide dismutase-1. Furthermore, upregulation of GPX4 by ginsenoside Re was mediated by phosphoinositide 3-kinase and extracellular signal-regulated kinase but not by p38 mitogen-activated protein kinase or c-Jun N-terminal kinase. Ginsenoside Re also suppressed 6-OHDA-triggered cellular accumulation of reactive oxygen species and peroxidation of membrane lipids. The GPX4 inhibitor (1S,3R)-RSL3 reversed ginsenoside Re-mediated inhibition of cellular damage in SH-SY5Y cells exposed to 6-OHDA, indicating that the neuronal activity of ginsenoside Re is due to upregulation of GPX4. These findings suggest that ginsenoside Re-dependent upregulation of GPX4 reduces oxidative stress and thereby alleviates 6-OHDA-induced neuronal damage.

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Section: Ginsenoside Re Attenuates 6-ohda-triggered Cellular Damagesupporting

confidence: 89%

Section: Ginsenoside Re Upregulates the Expression Of Gpx4mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ginsenoside Re Mitigates 6-Hydroxydopamine-Induced Oxidative Stress through Upregulation of GPX4

Lee

Hur

et al. 2020

Molecules

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“…ROS-mediated DA oxidation is also involved in microglial activation and dopaminergic cell death in the substantia nigra [ 51 ]. Besides, oxidative stress-mediated dopaminergic cell death is a major characteristic in toxin-induced PD models [ 52 , 53 ]. In this study, JSE, the water-soluble extract of JS, showed the excellent antioxidant activity of ROS/NO generation and MAO-B inhibitory activity in vitro compared to ginkgo leaf extract that is a known natural MAO-B inhibitor [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

In Vitro and in Vivo Neuroprotective Effects of Walnut (Juglandis Semen) in Models of Parkinson’s Disease

Choi

Park

Kim

et al. 2016

IJMS

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Monoamine oxidase (MAO) catalyzes the oxidative deamination of monoamines including dopamine (DA). MAO expression is elevated in Parkinson’s disease (PD). An increase in MAO activity is closely related to age, and this may induce neuronal degeneration in the brain due to oxidative stress. MAO (and particularly monoamine oxidase B (MAO-B)) participates in the generation of reactive oxygen species (ROS), such as hydrogen peroxide that are toxic to dopaminergic cells and their surroundings. Although the polyphenol-rich aqueous walnut extract (JSE; an extract of Juglandis Semen) has been shown to have various beneficial bioactivities, no study has been dedicated to see if JSE is capable to protect dopaminergic neurons against neurotoxic insults in models of PD. In the present study we investigated the neuroprotective potential of JSE against 1-methyl-4-phenylpyridinium (MPP+)- or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicities in primary mesencephalic cells and in a mouse model of PD. Here we show that JSE treatment suppressed ROS and nitric oxide productions triggered by MPP+ in primary mesencephalic cells. JSE also inhibited depletion of striatal DA and its metabolites in vivo that resulted in significant improvement in PD-like movement impairment. Altogether our results indicate that JSE has neuroprotective effects in PD models and may have potential for the prevention or treatment of PD.

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“…Thus, we may expect that restoration of dopamine (DA) synthesis and secretion levels may help to ameliorate the PD patients’ symptoms. Furthermore, it is suggested that mitochondrial dysfunction and the associated oxidative stress is the main mechanism responsible for neurodegeneration in PD [77]. DAergic neurons are particularly prone to oxidative damage due to high levels of inherent reactive oxygen species that are produced during DA synthesis or its breakdown by monoamine oxidases [78–79].…”

Section: Hif-1 and Parkinson’s Disease (Pd)mentioning

confidence: 99%

Hypoxia Inducible Factor-1 as a Target for Neurodegenerative Diseases

Zhang

Yan

Chang

et al. 2011

CMC

144

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Hypoxia inducible factor-1 (HIF-1) is a transcriptional factor responsible for cellular and tissue adaption to low oxygen tension. HIF-1, a heterodimer consisting of a constitutively expressed β subunit and an oxygen-regulated α subunit, regulates a series of genes that participate in angiogenesis, iron metabolism, glucose metabolism, and cell proliferation/survival. The activity of HIF-1 is controlled by post-translational modifications on different amino acid residues of its subunits, mainly the alpha subunit. Besides in ischemic stroke (see review [1]), emerging evidence has revealed that HIF-1 activity and expression of its down-stream genes, such as vascular endothelial growth factor and erythropoietin, are altered in a range of neurodegenerative diseases. At the same time, experimental and clinical evidence has demonstrated that regulating HIF-1 might ameliorate the cellular and tissue damage in the neurodegenerative diseases. These new findings suggest HIF-1 as a potential medicinal target for the neurodegenerative diseases. This review focuses on HIF-1α protein modifications and HIF-1’s potential neuroprotective roles in Alzheimer’s (AD), Parkinson’s (PD), Huntington’s diseases (HD), and amyotrophic lateral sclerosis (ALS).

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Therapeutic Effects of Hydrogen in Animal Models of Parkinson's Disease

Cited by 12 publications

References 89 publications

Ginsenoside Re Mitigates 6-Hydroxydopamine-Induced Oxidative Stress through Upregulation of GPX4

Ginsenoside Re Mitigates 6-Hydroxydopamine-Induced Oxidative Stress through Upregulation of GPX4

In Vitro and in Vivo Neuroprotective Effects of Walnut (Juglandis Semen) in Models of Parkinson’s Disease

Hypoxia Inducible Factor-1 as a Target for Neurodegenerative Diseases

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