Anticonvulsant action of celecoxib (alone and in combination with
sub-threshold dose of phenytoin) in electroshock induced convulsion

Shafiq, Nusrat; Malhotra, Supriya D.; Pandhi, P

doi:10.1358/mf.2003.25.2.723681

Cited by 39 publications

(28 citation statements)

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“…10,11 A study done by Shafiq et al reported findings of MES test which were comparable to the present study (Table 3). 22 Results from the current study were found to be in concordance with earlier reports of similar studies, most of them reporting anticonvulsant effects of COX-2 inhibitors on induced seizures in animals. Dhir et al reported that rofexocib, another COX-2 inhibitor has anticonvulsant effects on mice.…”

supporting

confidence: 93%

Evaluation of anticonvulsant effect of celecoxib, a selective cyclooxygenase-2 inhibitor in experimentally induced convulsions in albino rats

Nadeem

Maqdoom

2016

Int J Basic Clin Pharmacol

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supporting

confidence: 93%

Evaluation of anticonvulsant effect of celecoxib, a selective cyclooxygenase-2 inhibitor in experimentally induced convulsions in albino rats

Nadeem

Maqdoom

2016

Int J Basic Clin Pharmacol

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“…The effects of these seizures on transporter expression were attenuated when the rats were pretreated with indomethacin. This nonselective COX-1/ COX-2 inhibitor was used in these in vivo experiments because it does not affect seizure severity in the pilocarpine model (Ikonomidou-Turski et al, 1988), whereas celecoxib has been reported to have both pro-and anticonvulsant effects in epilepsy models (Baik et al, 1999;Shafiq et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Seizure-Induced Up-Regulation of P-Glycoprotein at the Blood-Brain Barrier through Glutamate and Cyclooxygenase-2 Signaling

Bauer

Hartz²,

Pekcec³

et al. 2007

Mol Pharmacol

253

301

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Increased expression of drug efflux transporters at the bloodbrain barrier accompanies epileptic seizures and complicates therapy with antiepileptic drugs. This study is concerned with identifying mechanistic links that connect seizure activity to increased P-glycoprotein expression at the blood-brain barrier. In this regard, we tested the hypothesis that seizures increase brain extracellular glutamate, which signals through an N-methyl-D-aspartate (NMDA) receptor and cyclooxygenase-2 (COX-2) in brain capillaries to increase blood-brain barrier P-glycoprotein expression. Consistent with this hypothesis, exposing isolated rat or mouse brain capillaries to glutamate for 15 to 30 min increased P-glycoprotein expression and transport activity hours later. These increases were blocked by 5H-dibenzo[a,d]cyclohepten-5,10-imine (dizocilpine maleate) (MK-801), an NMDA receptor antagonist, and by celecoxib, a selective COX-2 inhibitor; no such glutamate-induced increases were seen in brain capillaries from COX-2-null mice. In rats, intracerebral microinjection of glutamate caused locally increased P-glycoprotein expression in brain capillaries. Moreover, using a pilocarpine status epilepticus rat model, we observed seizure-induced increases in capillary P-glycoprotein expression that were attenuated by administration of indomethacin, a COX inhibitor. Our findings suggest that brain uptake of some antiepileptic drugs can be enhanced through COX-2 inhibition. Moreover, they provide insight into one mechanism that underlies drug resistance in epilepsy and possibly other central nervous system disorders.Up to 40% of epileptic patients respond poorly if at all to conventional pharmacotherapy, and impaired drug uptake into the brain is considered to be one important contributor to therapeutic failure Kwan and Brodie, 2006). Seizures are known to increase the expression of drug efflux transporters at the blood-brain barrier, and recent experiments in animal models of epilepsy show that brain uptake of antiepileptic drugs can be significantly improved by coadministration of tariquidar, a selective and potent inhibitor of the ATP-driven drug efflux pump, P-glycoprotein (Brandt et al., 2006;van Vliet et al., 2006). Together, these findings point to increased P-glycoprotein expression as one consequence of seizure activity that limits pharmacotherapy with antiepileptic drugs.The present study is concerned with mechanistic links that connect seizure activity to increased P-glycoprotein expression. Our goals are to identify therapeutic targets that can be manipulated to prevent seizure-induced transporter overexpression and to improve pharmacotherapy with antiepileptic drugs. The combined in vitro/in vivo experiments are focused

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“…COX-2 inhibitors such NS-398, indomethacin, diclofenac and celecoxib aggravated significantly seizure activity in animal model, especially kainic acid-induced seizure model (Baik et al, 1999). There were some evidences, in which Shafiq et al (2003) showed that there was an increase in percentage protection when celecoxib was combined with standard antiepileptic drug such as phenytoin against electroshock-induced convulsions (Samini et al, 2005). Tu and Bazan (2003) also demonstrated that the COX-2-selective inhibitor nimesulide attenuated kindling development (Tu and Bazan, 2005).…”

Section: Resultsmentioning

confidence: 99%

“…In the other studies, effects of COX2 inhibitor on seizure activity are different according to seizure models, types of NSAIDs and methods of administration (Dhir et al, 2005;Yuhas et al, 2005). In electroshock convulsion, celecoxib showed anticonvulsant action (Shafiq et al, 2003) and also posttreatment of celecoxib improved learning and memory deficit (Gobbo and O'Mara, 2004). Nimesulide and rofecoxib were reported to aggravate kainic acid-induced seizures and reduce the cell loss.…”

Section: Resultsmentioning

confidence: 99%

“…PGE2 activated on the electroencephalogram, while prostaglandin E1inhibit pentylenetetrazole-induced convulsions in rats (Kim et al, 2008). The drugs that inhibit COX-2 activity, such as indomethacin and selective COX-2 inhibitors, could reduce hippocampal cell death and seizure frequencies in several animal models of epilepsy (Jung et al, 2006;Kunz and Oliw, 2001a;Shafiq et al, 2003). Thus, drugs that reduce the production of PGs may have useful therapeutic effects in epilepsy.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Phenylbutazone on Pentylenetetrazole-Induced Seizure in Mice

Mirhadi¹

2011

American Journal of Animal and Veterinary Sciences

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Problem statement: The Cyclooxygenases (COXs), the key enzymes that convert arachidonic acid to Prostaglandins (PGs), had been implicated in physiological and pathophysiological functions in the CNS. Non-Stesoidal Anti-Inflammatory Drugs (NSAIDs), COX inhibitors, were used largely to treat febrile condition, pain state and for prevention of and therapeutics of many diseases. However the role of PGs and NSAIDs in the seizure activity has been disputed. The aim of this study was to evaluation the effect of intraperitoneally injection of different doses of Phenylbutazone on PTZinduced seizure threshold in mice. Approach: Mice were divided into 9 groups randomly: The first group received saline normal (ip) (control group); the second group received Carboxy Methyl Cellulose (CMC) 0.5% (ip) (vehicle group) and the next groups received respectively different doses of Phenylbutazone (5, 10, 20, 40, 60, 80 and 100 mg kg −1 ip) 45 min before determination of seizure threshold induced by PTZ. Results: Results showed that PTZ-induced seizure threshold in control mice was 34.75±1.54 mg kg −1 . Intraperitoneal injection of Phenylbutazone showed significant (p<0.05) increase of PTZ-induced seizure threshold in a dose dependently manner compared with control group. Conclusion: Phenylbutazone has anticonvulsant effects on mice. Nevertheless, new studies must be carried out in order to determine the beneficial effects of NSAIDs in treatment of epilepsy.

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Anticonvulsant action of celecoxib (alone and in combination with sub-threshold dose of phenytoin) in electroshock induced convulsion

Cited by 39 publications

References 0 publications

Evaluation of anticonvulsant effect of celecoxib, a selective cyclooxygenase-2 inhibitor in experimentally induced convulsions in albino rats

Evaluation of anticonvulsant effect of celecoxib, a selective cyclooxygenase-2 inhibitor in experimentally induced convulsions in albino rats

Seizure-Induced Up-Regulation of P-Glycoprotein at the Blood-Brain Barrier through Glutamate and Cyclooxygenase-2 Signaling

Effect of Phenylbutazone on Pentylenetetrazole-Induced Seizure in Mice

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