Riluzole reduces brain lesions and improves neurological function in rats after a traumatic brain injury

Wahl, Florence; Renou, Emmanuelle; Mary, Véronique; Stutzmann, Jean‐Marie

doi:10.1016/s0006-8993(97)00144-3

Cited by 72 publications

(39 citation statements)

References 54 publications

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“…The prepared samples were examined under BX.50 Olympus light microscope with Sony DXC-390P camera attached. Neuron degeneration, haemorrhage, oedema and inflammatory cell ratios in preparations were examined by modifying according to the scala developed by Wahl et al (19). In the scoring of injury, the ratio of injured region to the whole area was calculated and scoring was made as follows: 0 point in case of no injury, 1 point for injury of less than 25%, 2 points for injuries between 25%-75%, and 3 points for injuries between 75%-100%.…”

Section: Methodsmentioning

confidence: 99%

Neuroprotective effect of acute interferon-beta 1b treatment after spinal cord injury

Sengul¹,

Çoban²,

Çakır³

et al. 2012

Turkish Neurosurgery

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AIm: The purpose of this trial was to investigate the effect of a well known immunomodulator -interferon beta-on traumatized spinal cord in terms of biochemical and histopathological features. mAterIAl and methOds: Twenty-four rats were used in this trial. The rats were divided into 3 groups. In the first group of rats, spinal cord injury was created by the weight drop method and interferon beta was administered. In the second group, physiological saline was administered. Third group was used as control. Rats were sacrificed 24 hours following trauma. Heat shock protein 70 levels were measured in the spinal cord samples and the samples were examined histopathologically.results: When the rats in the physiological saline and control groups were compared to rats treated with interferon beta 1b, those treated with interferon beta 1b revealed significant increases in the heat shock protein 70 levels in tissues, and histopathological examination revealed decreases in polymorphonuclear leucocyte infiltration, haemorrhage, oedema and necrosis.COnClusIOn: Although, the results of the study indicated that interferon beta might have some healing effects via increasing the cellular heat shock protein 70 on spinal cord injuries, more studies are needed. KeywOrds:Heat shock protein 70, Interferon beta, Spinal cord injury ÖZ AmAÇ: Bu çalışmanın amacı, immunomodülatör olduğu bilinen interferon betanın travmaya uğramış omurilikteki etkisini biyokimyasal ve histopatolojik olarak araştırmaktır. yÖntem ve GereÇler: Bu çalışmada, 24 adet rat kullanıldı. Ratlar rastgele 3 gruba ayrıldı. Birinci gruptaki ratlarda ağırlık düşürme yöntemi ile omurilik travması oluşturularak interferon beta verildi. İkinci gruptaki ratlarda serum fizyolojik verildi. Üçüncü grup kontrol olarak kullanıldı. Denekler travmadan 24 saat sonra sakrifiye edildi. Alınan omurilik örneklerinde ısı şok proteini 70 düzeyleri ölçüldü ve örnekler histopatolojik olarak incelendi.BulGulAr: İnterferon beta 1b ile tedavi edilen ratlarda doku düzeyinde ısı şok proteini 70 düzeyinin serum fizyolojik verilen ratlara ve kontrollere göre belirgin olarak arttığı ve histopatolojik olarak polimorfonüklear lökosit infiltrasyonun, hemorajinin, ödemin ve nekrozun azaldığı gözlendi. sOnuÇ: Çalışmadan elde edilen veriler, interferon betanın travmatik omurilik yaralanmasında hücre seviyesinde ısı şok proteini 70 i artırarak iyileştirici etkisi olabileceğini göstermekle beraber daha ileri çalışmalara ihtiyaç vardır.AnAhtAr sÖZCÜKler: Isı şok proteini 70, İnterferon beta, Omurilik yaralanması

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Section: Methodsmentioning

confidence: 99%

Neuroprotective effect of acute interferon-beta 1b treatment after spinal cord injury

Sengul¹,

Çoban²,

Çakır³

et al. 2012

Turkish Neurosurgery

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“…Clinical development was halted in 2001. Riluzole is another drug in the same class that has been shown to reduce infarct volumes and improve behavioural outcomes in ischaemic injury [124,216] and traumatic brain injury [217,232]. Riluzole is currently indicated for use in ALS [136], but no clinical trials for stroke or traumatic brain injury are currently underway.…”

Section: Glutamate Release Blockersmentioning

confidence: 99%

Glutamate receptors, neurotoxicity and neurodegeneration

Lau¹,

Tymianski²

2010

Pflugers Arch - Eur J Physiol

1,020

697

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Glutamate excitotoxicity is a hypothesis that states excessive glutamate causes neuronal dysfunction and degeneration. As glutamate is a major excitatory neurotransmitter in the central nervous system (CNS), the implications of glutamate excitotoxicity are many and far-reaching. Acute CNS insults such as ischaemia and traumatic brain injury have traditionally been the focus of excitotoxicity research. However, glutamate excitotoxicity has also been linked to chronic neurodegenerative disorders such as amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease and others. Despite the continued research into the mechanisms of excitotoxicity, there are currently no pharmacological interventions capable of providing significant neuroprotection in the clinical setting of brain ischaemia or injury. This review addresses the current state of excitotoxic research, focusing on the structure and physiology of glutamate receptors; molecular mechanisms underlying excitotoxic cell death pathways and their interactions with each other; the evidence for glutamate excitotoxicity in acute neurologic diseases; laboratory and clinical attempts at modulating excitotoxicity; and emerging targets for excitotoxicity research.

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“…Axonolysis, axon degeneration, edema, hemorrhage, and inflammation were graded as 0, 1, 2, or 3 according to a modified grading system described by Wahl et al (22) (Table I). A light microscope with both 20x and 40x magnification was used in evaluating the histopathologic specimens, and final grades of axonolysis, axon degeneration, edema, hemorrhage, and inflammation were obtained for all of the nerves.…”

Section: Ii-statistical Examinationmentioning

confidence: 99%

Neuroprotective effects of agmatine in experimental peripheral nerve injury in rats: a prospective randomized and placebo-controlled trial

Sezer

Güçlü²,

Kazanci³

et al. 2013

Turkish Neurosurgery

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AIm:The purpose of this study was to demonstrate the activity of agmatine, an inducible nitric oxide synthase (iNOS) inhibitor and selective N-methyl-D-aspartate receptor (NMDAR) antagonist, on reducing tissue damage in distal part of traumatic nerve in an experimental rat peripheral nerve injury model. mATeRIAL and meTHods: Sciatic nerves of 30 Sprague Dawley male rats were used. Rats were divided into 5 groups; group 1 (n=6), control group; group 2 (n=6), axonotmesis + placebo group; group 3 (n=6), axonotmesis + 50 mg/kg agmatine treatment group; group 4 (n=6), neurotmesis + placebo group; group 5 (n=6), neurotmesis + 50 mg/kg agmatine treatment group. Axonolysis, axon degeneration, edema, hemorrhage, and inflammation were evaluated in histopathologic examinations of all the groups.ResuLTs: When group 2 was compared with group 3 in histopathologic sections, axonolysis was less in group 3 (p=0.007), as was axon degeneration (p=0.022) and edema (p=0.018). When group 4 was compared with group 5, axonolysis was less in group 5 (p=0.009), as was axon degeneration (p=0.006) and edema (p=0.021). CoNCLusIoN:This study demonstrated agmatine to have antioxidant and antineurotoxic effects in an experimental rat peripheral nerve injury model. KeywoRds: Agmatine, Axonotmesis, Neurotmesis, Peripheral nerve injury, Rat ÖZ AmAÇ: Bu çalışmanın amacı, indüklenebilir nitrik oksit sentetaz inhibitörü (iNOS) ve selektif N-metil-D-aspartat reseptörü (NMDAR) antagonisti olan agmatinin sıçanlarda yapılan deneysel periferik sinir yaralanma modelinde hasarlı sinirin distal bölumündeki doku hasarını azaltmadaki etkisini göstermekti. yÖNTem ve GeReÇLeR: Otuz tane Sprague Dawley sıçanının siyatik sinirleri kullanıldı. Sıçanlar beş gruba bölündü: birinci grup (n=6), kontrol grubu; ikinci grup (n=6), aksonotmezis + plasebo grubu; üçüncü grup (n=6), aksonotmezis + 50 mg/kg agmatin tedavi grubu; dördüncü Grup (n=6), neurotmesis + plasebo grubu; beşinci grup (n=6), neurotmesis + 50 mg/kg agmatin tedavi grubu. Aksonolizis, akson dejenerasyonu, ödem, hemoraji ve inflammasyon bütün gruplarda histopatolojik olarak değerlendirildi.BuLGuLAR: İkinci grup ile üçüncü grup histopatolojik kesitlerde kıyasladığında, aksonolizis üçüncü grupta daha azdı (p=0,007), aynı şekilde akson dejenerasyonu (p=0,022) ve ödem (p=0,018) üçüncü grupta daha azdı. Dördüncü grup ile beşinci grup histopatolojik kesitlerde kıyasladığında, aksonolizis beşinci grupta daha azdı (p=0,009), aynı şekilde akson dejenerasyonu (p=0,006) ve ödem (p=0,021) beşinci grupta daha azdı. soNuÇ: Bu çalışma, agmatinin sıçanlarda yapılan deneysel periferik sinir yaralanmalarında antioksidan ve antinörotoksik etkileri olduğunu göstermiştir.

show abstract

Riluzole reduces brain lesions and improves neurological function in rats after a traumatic brain injury

Cited by 72 publications

References 54 publications

Neuroprotective effect of acute interferon-beta 1b treatment after spinal cord injury

Neuroprotective effect of acute interferon-beta 1b treatment after spinal cord injury

Glutamate receptors, neurotoxicity and neurodegeneration

Neuroprotective effects of agmatine in experimental peripheral nerve injury in rats: a prospective randomized and placebo-controlled trial

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