Inhibitory effect of free radical scavenger, MCI-186, in the increase of hydroxyl radical induced by iminodipropionitrile in rats

Nomoto, Nobuatsu

doi:10.1016/j.jns.2003.12.005

Cited by 15 publications

(9 citation statements)

References 20 publications

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“…Edaravone was also found in recent clinical trials to reduce ox‐LDL and S‐100B protein plasma levels after cerebral infarction (Uno et al 2005). The anti‐inflammatory effects of edaravone have been confirmed in ischemia‐reperfusion models (Ito et al 2005; Ninomiya et al 2002; Suzuki et al 2005a,b; Tahara et al 2005; Totsuka et al 2005) and in nonischemic models of inflammation in extracerebral organs (Kono et al 2003; Nomoto 2004; Tanaka et al 2005).…”

Section: Pharmacologymentioning

confidence: 95%

“…In a rat hind limb warm ischemia‐reperfusion model, edaravone reduced histological changes in the gastrocnemius and tibialis anterior muscles and protected muscular dysfunction (Irie et al 2004). In an animal model of the Gilles de la Tourette syndrome, edaravone decreased hydroxyl radical levels in rat brains (Nomoto 2004). Edaravone also improved the sensitivity of endothelial cells to acetylcholine in smokers (Jitsuiki et al 2004).…”

Section: Pharmacologymentioning

confidence: 99%

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The Novel Antioxidant Edaravone: From Bench to Bedside

Watanabe

Tahara

Todo

2008

Cardiovascular Therapeutics

204

129

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Over the last decade, important advances have been made to support the fact that reactive oxygen species (ROS) are generated and play a harmful role during the acute and late stages of cerebral ischemia. Several drugs, such as radical scavengers and antioxidants, have been evaluated in preclinical and clinical studies. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one; Radicut R , Mitsubishi Tanabe Pharma Corporation) is a novel antioxidant that is currently used in Japan for the treatment of patients in the acute stage of cerebral infarction. Edaravone scavenges ROS and inhibits proinflammatory responses after brain ischemia in animals and humans. In particular, postischemic inflammation, leading to brain edema and infarction due to neuronal damage and endothelial cell death, can be ameliorated by edaravone. In addition to these antistroke effects, edaravone has also been shown to prevent oxidative damage to various extracerebral organs. Therefore, in addition to its usefulness in the treatment of stroke, edaravone is expected to play an integral role in the treatment of many oxidative stress-related diseases.

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Section: Pharmacologymentioning

confidence: 95%

Section: Pharmacologymentioning

confidence: 99%

The Novel Antioxidant Edaravone: From Bench to Bedside

Watanabe

Tahara

Todo

2008

Cardiovascular Therapeutics

204

129

View full text Add to dashboard Cite

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“…The oxidative stress theory has gained popularity in the past decade with the onset of research into possible therapeutic agents. For example, the synthesized free radical scavenger, MCI-186, was found to significantly decrease hydroxyl radical levels and was hypothesized to be effective against TS in an animal model (Nomoto 2004). …”

Section: Introductionmentioning

confidence: 99%

Involvement of immunologic and biochemical mechanisms in the pathogenesis of Tourette’s syndrome

et al. 2011

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Tourette's syndrome is a neurodevelopmental disorder clinically characterized by multiple motor and phonic tics. It is likely that a neurobiological susceptibility to the disorder is established during development by the interaction of genetic, biochemical, immunological, and environmental factors. This study sought to investigate the possible correlation of several immunological and biochemical markers with Tourette's syndrome. Children with Tourette's syndrome attending a tertiary pediatric medical center from May 2008 to April 2010, and healthy age-matched control subjects underwent a comprehensive biochemical and immunological work-up. Demographic data were abstracted from the medical records. Findings were compared between the groups and analyzed statistically. Sixty-eight children with Tourette's syndrome (58 males, 85.3%) and 36 healthy children (25 males, 69.4%) were recruited. Compared with the control group, the Tourette's syndrome group had significantly higher levels of ferritin (p = 0.01) and hemoglobin (p = 0.02), a lower level of zinc (p = 0.05), and a lower percentage of non-ceruloplasmin copper (p = 0.01). Analysis of the immunological markers revealed no significant between-group differences in IgA, IgM or IgG; however, IgE and IgG-4 levels were significantly higher in the Tourette's syndrome group (p = 0.04 and p = 0.02, respectively). Children with Tourette's syndrome have high levels of biochemical indices of oxidative stress and the quantitative immunoglobulins. These findings add to the still-limited knowledge on the pathogenesis of Tourette's syndrome and may have implications for the development of novel therapeutic modalities.

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“…The activated microglia are known to produce potentially neurotoxic species, including pro‐inflammatory cytokines, arachidonic acid metabolites (eicosanoids and quinolinic acid) and oxygen‐derived free radicals [26]. Pre‐treatment with antioxidant drugs has been shown to protect animals against IDPN‐induced ECC syndrome [9,18–20,22]. Hydrocortisone has been shown to profoundly suppress arachidonic acid break‐down products [39], including quinolinic acid [54].…”

Section: Discussionmentioning

confidence: 99%

“…[7,11] focused on the histopathology of inner ear revealed a direct correlation between vestibular hair cell degeneration and the severity of IDPN‐induced behavioural deficits. On the other hand, neuropharmacological and biochemical studies implicated various neurotransmitters/neuromodulators [10,12–17] and oxygen‐derived free radicals [9,18–22] in the development of IDPN‐induced ECC syndrome.…”

mentioning

confidence: 99%

Protective Effect of Hydrocortisone on Iminodipropionitrile‐Induced Neurotoxicity in Rats

Tariq

Khan

Siddiquei

et al. 2007

Basic Clin Pharma Tox

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Occupational and environmental exposure of synthetic nitriles is of potential relevance to human health. Iminodipropionitrile (IDPN), a prototype nitrile toxin, has been shown to produce dyskinetic syndrome in rodents. This study reports the effect of concomitant exposure of rats to hydrocortisone and IDPN on behavioural abnormalities namely excitation, circling and chorea (ECC) syndrome. Four groups of female Wistar rats were given hydrocortisone (0, 10, 30 and 60 mg/kg, gavage, for 10 days) 30 min. before IDPN (100 mg/kg, intraperitoneally for 8 days). Two additional groups of rats were treated with either saline (control group) or 60 mg/kg of hydrocortisone (drug alone group). The animals were observed for neurobehavioural abnormalities including dyskinetic head movement, circling, tail hanging, air righting reflex and contact inhibition of righting reflex. After behavioural studies, the animals were killed, and the discrete brain regions and temporal bones were collected for biochemistry and inner ear histopathology, respectively. Hydrocortisone significantly and dose dependently attenuated the incidence and severity of IDPN-induced behavioural syndrome. Administration of hydrocortisone (60 mg/kg) alone significantly increased glutathione (GSH) levels in olfactory bulb and striatum, whereas IDPN alone significantly reduced GSH levels in olfactory bulb, striatum and hippocampus. Hydrocortisone (60 mg/kg) significantly compensated IDPN-induced depletions of GSH in different brain regions. Hydrocortisone also protected the animals against IDPN-induced vestibular hair cell degeneration. The protective effect of hydrocortisone may be attributed to its anti-inflammatory and antioxidant properties.

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Inhibitory effect of free radical scavenger, MCI-186, in the increase of hydroxyl radical induced by iminodipropionitrile in rats

Cited by 15 publications

References 20 publications

The Novel Antioxidant Edaravone: From Bench to Bedside

The Novel Antioxidant Edaravone: From Bench to Bedside

Involvement of immunologic and biochemical mechanisms in the pathogenesis of Tourette’s syndrome

Protective Effect of Hydrocortisone on Iminodipropionitrile‐Induced Neurotoxicity in Rats

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