Protective effect of the radical scavenger edaravone against methamphetamine-induced dopaminergic neurotoxicity in mouse striatum

Kawasaki, Toshiyuki; Ishihara, Kotaro; Ago, Yukio; Nakamura, Shigeo; Itoh, Soichi; Baba, Akemichi; Matsuda, Takehisa

doi:10.1016/j.ejphar.2006.05.012

Cited by 36 publications

(28 citation statements)

References 40 publications

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“…These findings suggest that reactive oxygen species and nitric oxide play a key role in MPTP-induced dopaminergic degeneration in the SNc, but not in the striatum. The finding that edaravone protects against only the nigral neurotoxicity seems to contrast with the previous observation that the drug blocks the striatal neurotoxicity in methamphetamine-treated mice (Kawasaki et al, 2006). This may be explained by the difference in the mechanism for neurotoxicity between methamphetamine and MPTP models.…”

Section: Discussioncontrasting

confidence: 55%

“…Banno et al (2005) revealed that edaravone suppressed the production of nitric oxide and reactive oxygen species by activated microglia. We have recently reported that edaravone protected methamphetamine-induced striatal dopaminergic neurotoxicity by scavenging peroxynitrite (Kawasaki et al, 2006). These findings suggest that edaravone may be effective in improving reactive oxygen species-or nitric oxide-mediated neurodegenerative disorders.…”

mentioning

confidence: 80%

“…The concentrations of dopamine were quantified by high-performance liquid chromatography (HPLC) with an electrochemical detector (ECD-100; Eicom, Kyoto, Japan) (Kawasaki et al, 2006). The brains of mice were quickly removed and dissected on an ice-cold glass plate.…”

Section: Animalsmentioning

confidence: 99%

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Edaravone (3-Methyl-1-phenyl-2-pyrazolin-5-one), a Radical Scavenger, Prevents 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Neurotoxicity in the Substantia Nigra but Not the Striatum

Kawasaki

Ishihara²,

Ago³

et al. 2007

J Pharmacol Exp Ther

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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes nigrostriatal dopaminergic neurotoxicity and behavioral impairment in rodents, and previous studies suggest that nitric oxide and reactive oxygen species are involved in MPTP-induced neurotoxicity. The present study examines the effect of edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a radical scavenger, on MPTP-induced neurotoxicity in the striatum and substantia nigra pars compacta (SNc) of C57BL/6J mice. MPTP treatment (10 mg/kg s.c. ϫ 4 with 2-h intervals) decreased dopamine levels and tyrosine hydroxylase immunostaining in the striatum and SNc. Pretreatment with edaravone (1 and 3 mg/kg i.p.) significantly reduced the neurotoxicity in the SNc but not striatum. An immunohistochemical study showed that MPTP caused microglial activation both in the striatum and SNc, whereas it increased 3-nitrotyrosine immunoreactivity, an in vivo biomarker of peroxynitrite production, in the SNc but not the striatum. Furthermore, MPTP increased lipid peroxidation product thiobarbituric acid reactive substance in the midbrain, but not the striatum. Edaravone inhibited activation of the microglia and the increased 3-nitrotyrosine immunoreactivity in the SNc but not the striatum, and it also inhibited thiobarbituric acid reactive substance levels in the midbrain. Behavioral analyses showed that edaravone improved MPTP-induced impairment of locomotion and Rotorod performance. These results suggest that edaravone protects against MPTP-induced neurotoxicity in the SNc by blocking the production of reactive oxygen species or peroxynitrite and imply that dopaminergic degeneration in the SNc may play an important role in MPTP-induced motor dysfunction of mice.

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Section: Discussioncontrasting

confidence: 55%

mentioning

confidence: 80%

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Edaravone (3-Methyl-1-phenyl-2-pyrazolin-5-one), a Radical Scavenger, Prevents 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Neurotoxicity in the Substantia Nigra but Not the Striatum

Kawasaki

Ishihara²,

Ago³

et al. 2007

J Pharmacol Exp Ther

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“…Edaravone markedly improved the survival rate of paraquattreated mice (92). In another animal model of toxin exposure, the administration of high doses of methamphetamine causes the degeneration of striatal dopaminergic fibers in the brains of rodents, and oxidative stress appears to be one of the main factors involved in the neurotoxic effects (93). Edaravone has been reported to protect mice against methamphetamineinduced neurotoxicity in the striatum by blocking peroxynitrite production (93).…”

Section: Toxin Exposurementioning

confidence: 99%

“…In another animal model of toxin exposure, the administration of high doses of methamphetamine causes the degeneration of striatal dopaminergic fibers in the brains of rodents, and oxidative stress appears to be one of the main factors involved in the neurotoxic effects (93). Edaravone has been reported to protect mice against methamphetamineinduced neurotoxicity in the striatum by blocking peroxynitrite production (93). Edaravone also blocked the increase in 3-nitrotyrosine immunoreactivity, a biomarker for ROS generation, and the activation of astrocytes (93).…”

Section: Toxin Exposurementioning

confidence: 99%

Beyond neurological disease: New targets for edaravone (Review)

Kikuchi¹,

Uchikado²,

Miyagi³

et al. 2011

Int J Mol Med

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Pathological Implications of Oxidative Stress in Patients and Animal Models with Schizophrenia: The Role of Epidermal Growth Factor Receptor Signaling

Nagano

Mizuno²,

Morita

et al. 2015

Current Topics in Behavioral Neurosciences

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Proinflammatory cytokines perturb brain development and neurotransmission and are implicated in various psychiatric diseases, such as schizophrenia and depression. These cytokines often induce the production of reactive oxygen species (ROS) and regulate not only cell survival and proliferation but also inflammatory process and neurotransmission. Under physiological conditions, ROS are moderately produced in mitochondria but are rapidly scavenged by reducing agents in cells. However, brain injury, ischemia, infection, or seizure-like neural activities induce inflammatory cytokines and trigger the production of excessive amounts of ROS, leading to abnormal brain functions and psychiatric symptoms. Protein phosphatases, which are involved in the basal silencing of cytokine receptor activation, are the major targets of ROS. Consistent with this, several ROS scavengers, such as polyphenols and unsaturated fatty acids, attenuate both cytokine signaling and psychiatric abnormalities. In this review, we list the inducers, producers, targets, and scavengers of ROS in the brain and discuss the interaction between ROS and cytokine signaling implicated in schizophrenia and its animal models. In particular, we present an animal model of schizophrenia established by perinatal exposure to epidermal growth factor and illustrate the pathological role of ROS and antipsychotic actions of ROS scavengers, such as emodin and edaravone.

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Protective effect of the radical scavenger edaravone against methamphetamine-induced dopaminergic neurotoxicity in mouse striatum

Cited by 36 publications

References 40 publications

Edaravone (3-Methyl-1-phenyl-2-pyrazolin-5-one), a Radical Scavenger, Prevents 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Neurotoxicity in the Substantia Nigra but Not the Striatum

Edaravone (3-Methyl-1-phenyl-2-pyrazolin-5-one), a Radical Scavenger, Prevents 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Neurotoxicity in the Substantia Nigra but Not the Striatum

Beyond neurological disease: New targets for edaravone (Review)

Pathological Implications of Oxidative Stress in Patients and Animal Models with Schizophrenia: The Role of Epidermal Growth Factor Receptor Signaling

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