Short-Term Administration of a New Free Radical Scavenger, Edaravone, Is More Effective Than its Long-Term Administration for the Treatment of Neonatal Hypoxic–Ischemic Encephalopathy

Noor, Jesmin I.; Ikeda, Tomoaki; Mishima, Kenichi; Aoo, Naoya; Ohta, Sumie; Egashira, Nobuaki; Iwasaki, Katsunori; Fujiwara, Michihiro; Ikenoue, Tsuyomu

doi:10.1161/01.str.0000185653.49740.c6

Cited by 48 publications

(36 citation statements)

References 28 publications

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“…In this connection, it is very interesting to consider DNA peroxidation from the standpoint of oxidation stress pathology. It is already reported that 2-d edaravone treatment is more effective than 5-d or 10-d treatment in this model (26). We also showed that 8-OHdG overexpression correlated to apoptotic neuronal cell death within 48 h after HI insult.…”

Section: Discussionsupporting

confidence: 74%

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Edaravone Inhibits DNA Peroxidation and Neuronal Cell Death in Neonatal Hypoxic-Ischemic Encephalopathy Model Rat

et al. 2009

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Neonatal hypoxic-ischemic encephalopathy (HIE) is the most frequent neurologic disease in the perinatal period. Its major cause is oxidative stress, which induces DNA peroxidation and apoptotic neuronal death. We examined 8-hydroxy-2Ј-deoxyguanosine (8-OHdG) expression to evaluate brain damage in neonatal HIE and the therapeutic effect of edaravone, a free radical scavenger. Using HPLC and immunohistochemistry, the 8-OHdG levels of neonatal HIE model Sprague-Dawley rats that were subjected to left common carotid artery ligation and 2-h hypoxia significantly increased after 24 -48 h of hypoxic-ischemic (HI) insult, but decreased after 72 h. Moreover, the number of apoptotic cells with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and karyorrhexis significantly increased after 24 -72 h of HI insult. In a therapeutic experiment, edaravone was administered i.p.

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Section: Discussionsupporting

confidence: 74%

“…The same dose of edaravone or normal saline was then administered every 24 h until being killed. The dose and time course of edaravone were based on the previous data (26). Rat pups were killed 6, 24, 48, and 72 h after HI insult.…”

Section: Methodsmentioning

confidence: 99%

Edaravone Inhibits DNA Peroxidation and Neuronal Cell Death in Neonatal Hypoxic-Ischemic Encephalopathy Model Rat

et al. 2009

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“…Interestingly, short term administration of this drug was reported to be more effective than its long term use [67].…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

Clinical and pharmacological aspects of bath salt use: A review of the literature and case reports

Miotto¹,

Striebel²,

Cho

et al. 2013

Drug and Alcohol Dependence

121

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Abstract:Reactive oxygen species (ROS) are widely believed to cause or aggravate several human pathologies such as neurodegenerative diseases, cancer, stroke and many other ailments. Antioxidants are assumed to counteract the harmful effects of ROS and therefore prevent or treat oxidative stress-related diseases. In this report, recent human studies exploring the efficiency of antioxidants in prevention and treatment of various diseases are reviewed. Few antioxidants including edaravone (for ischemic stroke in Japan), Nacetylcysteine (for acetaminophen toxicity), alfa-lipoic acid (for diabetic neuropathy) and some flavonoids (polyphenolic compounds present in dietary plants), such as micronized purified flavonoid fraction (diosmin and hesperidin) and oxerutins (for chronic venous insufficiency) as well as baicalein and catechins (for osteoarthritis) have found accepted clinical use. However, despite much enthusiasm in the 1980s and 1990s, many well-known agents such as antioxidant vitamins and also more recently developed compounds such as nitrones have not successfully passed the scrutiny of clinical trials for prevention and treatment of various diseases. This has given rise to a pessimistic view of antioxidant therapy, however, the evidence from human epidemiological studies about the beneficial effects of dietary antioxidants and preclinical in vitro and animal data are compelling. We have probably wasted too much time on agents like antioxidant vitamins instead of focusing on more disease specific, target-directed, highly bioavailable antioxidants. We here discuss possible reasons for the lack of success in some clinical trials and seek to provide some suggestions to be considered if antioxidant therapy is to succeed as an effective therapeutic strategy.

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“…If the animal succeeded in swimming to the platform within 120 s and stayed on the platform for 20 s, the animal was considered to have recognized the location of the platform, and the measurement was completed. For any animal which failed to swim to the platform within 120 s, the measurement was terminated, the goal latency was recorded as 120 s, and the animal was gently placed on the platform for 20 s. 9) Working Memory Test The animals were subjected to the Morris water maze test for working memory for 3 d, starting 2 d after the reference memory test. The working memory test was procedurally similar to the reference memory test, except that the platform location was fixed within the test day, but changed each test day.…”

Section: )mentioning

confidence: 99%

Neonatal Phencyclidine Treatment in Mice Induces Behavioral, Histological and Neurochemical Abnormalities in Adulthood

Nakatani-Pawlak

Yamaguchi²,

Tatsumi

et al. 2009

Biological & Pharmaceutical Bulletin

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N-Methyl-D-aspartate (NMDA)-type glutamic acid receptors play a critical role in excitatory synaptic transmission, synaptic plasticity and neuronal development in the central nervous system. During the developmental stage from week 25 of gestation to birth in humans, elongation and branching of axons and dendrites of nerve cells, synapse formation, myelination and realignment of nerve pathways (neural circuits) for acquiring higher neural function actively proceed, and this stage corresponds to postnatal weeks 1 through 2 in mice.1) It is generally recognized that non-synapse-mediated intercellular glutamic acid is largely involved in this process of nerve development. Stimulation of NMDA receptors facilitated radial migration of the cortical plate of excitatory nerve cells 2) and the selective blockade of NMDA receptors disturbed neuronal migration in the cerebral cortex.3)It has been reported that rats injected subcutaneously (s.c.) with phencyclidine (PCP), a noncompetitive NMDA receptor antagonist, at 10 mg/kg once a day during the postnatal development stage (postnatal days 7, 9 and 11) exhibit an increase in spontaneous motor activity, impairment of prepulse inhibition and behavioral changes in respect of learning and cognition after attaining maturation.4-7) When rats neonatally administered PCP were examined for any changes in the binding capacity of NMDA receptors and g-aminobutyrate A (GABA A ) receptors at maturity by autoradiography using In the present study, we investigated brain function from the behavioral, anatomical and neurochemical viewpoints in mice injected with PCP at 10 mg/kg on postnatal days 7, 9 and 11. Especially, we focused on changes in social interaction in PCP-treated mice, and examined the effects of clozapine, an atypical antipsychotic drug, D-cycloserine, an NMDA receptor partial agonist, flumazenil, a benzodiazepine receptor antagonist, and SHC50911, a GABA B receptor antagonist on social interaction deficits in PCP-treated mice. Of note, as far as we are aware, this is the first experimental demonstration that neonatal PCP treatment in mice results in increased sensitivity to PCP, and impaired social interaction behaviors in adulthood, which are accompanied by a decrease in the number of GABAergic interneurons and spine density in the frontal cortex and hippocampus, and abnormal monoamine metabolism in the brain. Neonatal PCP treatment in mice could be regarded as a neurodevelopmental animal model for schizophrenia. MATERIALS AND METHODSMethods. Animals Male mice aged 13 weeks old and female mice aged 13 weeks old Crlj:CD1 (ICR) were mated, and male offspring were used on postnatal day 7. Animals were maintained in a room controlled at 23°C and 55% humidity with a 12-h lighting cycle (lights on: 6:00 a.m.), and 12 ventilations/h. Animals had free access to solid feed (CRF-1; Oriental Yeast Co., Ltd., Tokyo, Japan) from feed- Kakuma-machi, Kanazawa 920-1192, Japan: b Nihon Bioresearch Inc.; 6-104 Majima, Fukuju-cho, Hashima, Gifu 501-6251, Japan: c Narabyouri Research Co.,...

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Short-Term Administration of a New Free Radical Scavenger, Edaravone, Is More Effective Than its Long-Term Administration for the Treatment of Neonatal Hypoxic–Ischemic Encephalopathy

Cited by 48 publications

References 28 publications

Edaravone Inhibits DNA Peroxidation and Neuronal Cell Death in Neonatal Hypoxic-Ischemic Encephalopathy Model Rat

Edaravone Inhibits DNA Peroxidation and Neuronal Cell Death in Neonatal Hypoxic-Ischemic Encephalopathy Model Rat

Clinical and pharmacological aspects of bath salt use: A review of the literature and case reports

Neonatal Phencyclidine Treatment in Mice Induces Behavioral, Histological and Neurochemical Abnormalities in Adulthood

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