NMDA Receptor Antagonist Felbamate Reduces Behavioral Deficits and Blood–Brain Barrier Permeability Changes after Experimental Subarachnoid Hemorrhage in the Rat

Germanò, Antonino; Caffo, Maria; Angileri, Filippo Flavio; Arcadi, Francesca Antonia; Newcomb-Fernandez, Jennifer; Caruso, Gerardo; Meli, Francesco; Pineda, José; Lewis, Stephen B.; Wang, Kevin; Bramantı, Placido; Costa, Chiara; Hayes, Ronald L.

doi:10.1089/neu.2006.0181

Cited by 55 publications

(55 citation statements)

References 65 publications

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“…Moreover, it has been shown that the NMethyl-D-aspartic (NMDA) receptors antagonist, Felbamate, leads to an improved neurological performance and limits the BBB breakdown in the single-injection rat model of SAH [55]. This finding is consistent with the results of the current study.…”

Section: Discussionsupporting

confidence: 92%

The Effect of Blood Glutamate Scavengers Oxaloacetate and Pyruvate on Neurological Outcome in a Rat Model of Subarachnoid Hemorrhage

et al. 2012

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Section: Discussionsupporting

confidence: 92%

The Effect of Blood Glutamate Scavengers Oxaloacetate and Pyruvate on Neurological Outcome in a Rat Model of Subarachnoid Hemorrhage

et al. 2012

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“…2,21,27 It has long been known that glutamate is detrimental to neurons following SAH. 9,16,34 In an in vitro study, baicalein has been demonstrated to have a protective effect against glutamate-induced neurotoxicity. 17 In the present in vivo study, we also found that brain neurons can be protected against SAH though either direct attenuation of glutamate surge or by oxidative stress inhibition.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of neurological injury with early baicalein treatment following subarachnoid hemorrhage in rats

Kuo¹,

Chen³

et al. 2013

JNS

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ObjectBaicalein has been shown to offer neuroprotection in the ischemic brain, but its effect in subarachnoid hemorrhage (SAH) is unknown. The authors used a double-hemorrhage model to study the role of early baicalein treatment in SAH.MethodsSubarachnoid hemorrhage was induced in male Wistar rats through a repeat injection of autologous blood at a 48-hour interval. Rats subjected or not subjected to SAH received a 30-mg/kg baicalein injection 3 hours after SAH and daily for 6 consecutive days, and results were compared with those obtained in vehicle-treated control rats. Mortality of the rats was recorded. Neurological outcome was assessed daily. Cerebrospinal fluid dialysates were collected and examined for glutamate concentrations. Cerebral vasospasm (CVS), brain water content, neuron variability, expression of glutamate transporter–1 (GLT-1), immunoreactivity of astrocyte, and level of malondialdehyde, activities of superoxide dismutase (SOD), and catalase in brain tissues content were determined on post-SAH Day 7.ResultsMortality rate, neuronal degeneration, brain water content, and CVS were decreased and neurological function improved in the baicalein-treated rats. Baicalein increased astrocyte activity and preserved GLT-1, which attenuated the glutamate surge after SAH. Baicalein also provided antioxidative stress by preserving activities of SOD and catalase and decreased malondialdehydelevel after SAH. The glutamate, body weight, neurological scores, and glial fibrillary acidic protein activity were significantly correlated. The CVS was correlated with neuronal degeneration, and GLT-1 was correlated with oxidative stress.ConclusionsEarly baicalein treatment attenuated CVS and limited neurological injury following SAH. These data may indicate clinical utility for baicalein as an adjunct therapy to reduce brain injury and improve patient outcomes.

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“…Germano et al 26 showed that N-methyl-D-aspartate excitotoxicity is involved in the central dysfunction after SAH, and a N-methyl-D-aspartate receptor antagonist reduced behavioral deficits. In our previous study, an increase in glutamate level, down-regulation of GLT-1 expression, and neuronal degeneration were also observed after SAH.…”

Section: Critical Care Medicinementioning

confidence: 99%

“…3,14,15,32,33 A pharmacokinetic study conducted with mice showed a plasma curcumin concentration of 2.25 g/ml after 15 min after intraperitoneal administration of 100 mg/kg curcumin and a brain curcumin concentration of 0.41 g/g after 1 h. 37 Disruption of the blood-brain barrier after SAH has been reported. 26 In this condition, the permeability of the brain to curcumin may be higher than normal. Further investigation is needed to associate the duration of the neuroprotective effect of curcumin after brain injury with the dosage administered.…”

Section: -4mentioning

confidence: 99%

Neuroprotective Effect of Curcumin in an Experimental Rat Model of Subarachnoid Hemorrhage

Kuo

Wen

et al. 2011

Anesthesiology

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NMDA Receptor Antagonist Felbamate Reduces Behavioral Deficits and Blood–Brain Barrier Permeability Changes after Experimental Subarachnoid Hemorrhage in the Rat

Cited by 55 publications

References 65 publications

The Effect of Blood Glutamate Scavengers Oxaloacetate and Pyruvate on Neurological Outcome in a Rat Model of Subarachnoid Hemorrhage

The Effect of Blood Glutamate Scavengers Oxaloacetate and Pyruvate on Neurological Outcome in a Rat Model of Subarachnoid Hemorrhage

Attenuation of neurological injury with early baicalein treatment following subarachnoid hemorrhage in rats

Neuroprotective Effect of Curcumin in an Experimental Rat Model of Subarachnoid Hemorrhage

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