Involvement of endogenous prostaglandin F2α on kainic acid-induced seizure activity through FP receptor: The mechanism of proconvulsant effects of COX-2 inhibitors

Kim, Hee-Jae; Chung, Jae Ho; Lee, Soo Hwan; Jung, Yi‐Sook; Moon, Chang-Hyun; Baik, Eun Joo

doi:10.1016/j.brainres.2007.12.017

Cited by 80 publications

(54 citation statements)

References 37 publications

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“…Ibuprofen also induced the learning and memory deficit. These cumulated data shows that NSAID including COX-2 inhibitors might be harmful especially in seizure conditions (Kim et al, 2008).…”

Section: Resultsmentioning

confidence: 90%

“…Non-Stesoidal Anti-Inflammatory Drugs (NSAIDs), COX inhibitors, are 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 (Kim et al, 2008). The enzyme exists as constitutive (COX-1) and inducible (COX-2) isoforms, being the latter a major player in inflammation (Minghetti and Pocchiari, 2007).…”

Section: Introductionmentioning

confidence: 99%

“…It was found that COX-2 regulates cell membrane excitability and long term synaptic plasticity in the hippocampus (Chen and Bazan, 2005), suggesting that COX-2 may play a critical role in convulsive states. However, results of previous studies about the role of COX-2 in the genesis and maintenance of convulsion are controversial; for instance both proconvulsant and anticonvulsant role for COX-2 has been reported in kainic acid-induced seizure (Kim et al, 2008). Also, overexpression of COX-2 has been associated with neurotoxiticy in acute conditions, such as hypoxia/ischemia and seizures, as well as in chronic neurodegenerative diseases, including amyotrophic lateral sclerosis, Parkinson's disease and Alzheimer's disease (Minghetti and Pocchiari, 2007).…”

Section: Introductionmentioning

confidence: 99%

“…Effect of COX inhibitors which are suggested to prevent the production of PGs during seizure activity, were inconsistent according to seizure models, types of COX inhibitors, or time of administration. Thus, the role of COX isozymes or PGs in seizure activity is not clear (Kim et al, 2008). During kainic acid-induced seizure, the PGF2α, PGE2 and PGD2 was increased in the brain after a few minutes.…”

Section: Introductionmentioning

confidence: 99%

“…In convulsion-prone gerbil, the increase of PGD2 in the brain is significant and exogenous PGD2 inhibits pentylenetetrazole-induced convulsions. 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).…”

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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Section: Resultsmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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Pharmacological targeting of brain inflammation in epilepsy: Therapeutic perspectives from experimental and clinical studies

Ravizza

Vezzani

2018

Epilepsia Open

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SummaryIncreasing evidence supports a pathogenic role of unabated neuroinflammation in various central nervous system (CNS) diseases, including epilepsy. Neuroinflammation is not a bystander phenomenon of the diseased brain tissue, but it may contribute to neuronal hyperexcitability underlying seizure generation, cell loss, and neurologic comorbidities. Several molecules, which constitute the inflammatory milieu in the epileptogenic area, activate signaling pathways in neurons and glia resulting in pathologic modifications of cell function, which ultimately lead to alterations in synaptic transmission and plasticity. Herein we report the up‐to‐date experimental and clinical evidence that supports the neuromodulatory role of inflammatory mediators, their related signaling pathways, and involvement in epilepsy. We discuss how these mechanisms can be harnessed to discover and validate targets for novel therapeutics, which may prevent or control pharmacoresistant epilepsies.

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Neuronal and nonneuronal COX‐2 expression confers neurotoxic and neuroprotective phenotypes in response to excitotoxin challenge

Belevych

Wang

et al. 2013

J of Neuroscience Research

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Treating acute brain injuries with COX-2 inhibitors can produce both neuroprotective and neurotoxic effects. This study investigated the role of COX-2 in modulating acute brain injury induced by excitotoxic neural damage. Intrastriatal injection of excitotoxin (RS)-(tetrazole-5yl) glycine elicited COX-2 expression in two distinct groups of cells. cortical neurons surrounding the lesion and vascular cells in the lesion core. The vascular COX-2 was expressed in two cell types, endothelial cells and monocytes. Selective deletion of COX-2 in vascular cells in Tie2Cre Cox-2flox/flox mice did not affect the induction of COX-2 in neurons after the excitotoxin injection but resulted in increased lesion volume, indicating a neuroprotective role for the COX-2 expressed in the vascular cells. Selective deletion of monocyte COX-2 in LysMCre Cox-2flox/flox mice did not reduce COX-2-dependent neuroprotection, suggesting that endothelial COX-2 is sufficient to confer neuroprotection. Pharmacological inhibition of COX-2 activity in Tie2Cre Cox-2flox/flox mice reduced lesion volume, indicating a neurotoxic role for the COX-2 expressed in neurons. Furthermore, COX-2-dependent neurotoxicity was mediated, at least in part, via the activation of the EP1 receptor. These results show that Cox-2 expression induced in different cell types can confer opposite effects.

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Involvement of endogenous prostaglandin F2α on kainic acid-induced seizure activity through FP receptor: The mechanism of proconvulsant effects of COX-2 inhibitors

Cited by 80 publications

References 37 publications

Effect of Phenylbutazone on Pentylenetetrazole-Induced Seizure in Mice

Effect of Phenylbutazone on Pentylenetetrazole-Induced Seizure in Mice

Pharmacological targeting of brain inflammation in epilepsy: Therapeutic perspectives from experimental and clinical studies

Neuronal and nonneuronal COX‐2 expression confers neurotoxic and neuroprotective phenotypes in response to excitotoxin challenge

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