Systematic review of the role of prostaglandins and their synthetase inhibitors with respect to febrile seizures

Rantala, Heikki; Tarkka, Rita; Uhari, Matti

doi:10.1016/s0920-1211(01)00281-9

Cited by 15 publications

(13 citation statements)

References 34 publications

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“…Other evidence supporting the proconvulsive properties of PGF 2α include several cases of seizures and abnormal electroencephalographic changes associated with the clinical use of PGF 2α analogs to terminate pregnancy that have been reported in clinical practice [54-57]. Nevertheless, action PGF 2α is disputed and the FP receptor role still remains controversial [58]. Several contrary experimental reports demonstrated that administration of PGF 2α caused seizure aggravation [59] and abolished the anticonvulsant effects of other prostaglandins [60,61], whereas others suggested that elevated levels of PGF 2α might have anticonvulsant action [43,62].…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin F2α FP receptor antagonist improves outcomes after experimental traumatic brain injury

Glushakov

Robbins

Bracy

et al. 2013

J Neuroinflammation

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BackgroundInjuries to the brain promote upregulation of prostaglandins, notably the proinflammatory PGF2α, and overactivation of their cognate G-protein-coupled FP receptor, which could exacerbate neuronal damage. Our study is focused on investigation of the FP receptor as a target for novel neuroprotective drugs in a preclinical animal traumatic brain injury (TBI) model.MethodsAccordingly, the effects of acute intraperitoneal post-treatment with selective FP antagonist AL-8810 were studied in wildtype (WT) and FP receptor knockout (FP-/-) mice after controlled cortical impact (CCI). Neurological impairments were evaluated using neurological deficit scores (NDS) and the grip strength test. Cortical lesions and overall brain pathology were assessed using immunohistochemistry.ResultsMorphological analyses of cerebral vasculature and anastomoses revealed no differences between WT and FP-/- mice. CCI produced cortical lesions characterized by cavitation, neuronal loss, and hematoma with a volume of 20.0 ± 1.0 mm3 and significant hippocampal swelling (146.5 ± 7.4% of contralateral) compared with sham (P < 0.05). Post-treatment with AL-8810 (1 to 10 mg/kg) had no significant effect on cortical lesions, which suggests the irreversible effect of primary CCI injury, but significantly reduced hippocampal swelling to a size not significantly different from the sham group. Post-treatment with AL-8810 at a dose of 10 mg/kg significantly improved NDS at 24 and 48 hours after CCI (P < 0.001 and P < 0.01, respectively). In the AL-8810 group, CCI-induced decrease in grip strength was three-fold (2.93 ± 1.71) less and significantly different than in the saline-treated group. The FP-/- mice had significantly less hippocampal swelling, but not NDS, compared with WT mice. In addition, immunohistochemistry showed that pharmacologic blockade and genetic deletion of FP receptor led to attenuation of CCI-induced gliosis and microglial activation in selected brain regions.ConclusionThis study provides, for the first time, demonstration of the unique role of the FP receptor as a potential target for disease-modifying CNS drugs for treatment of acute traumatic injury.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin F2α FP receptor antagonist improves outcomes after experimental traumatic brain injury

Glushakov

Robbins

Bracy

et al. 2013

J Neuroinflammation

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“…PGs are known to markedly increase following seizures and may contribute to epileptogenesis and reduction in seizure threshold [10, 52]. Phospholipase A 2 liberates arachidonic acid from membrane phospholipids.…”

Section: Prostaglandin Production In Epilepsymentioning

confidence: 99%

“…Because PGs play an important role in inflammatory responses, the functions of PGs in epileptogenesis have been studied for a considerable amount of time [52, 54]; however, data on the roles of COX-2 in epilepsy appear to be bidirectional. For example, following an injection of kainic acid (KA), postseizure treatment with the selective COX-2 inhibitor NS-398 prevented neuronal cell loss in the hippocampus [55].…”

Section: Prostaglandin Production In Epilepsymentioning

confidence: 99%

Role of Inflammatory Mediators in the Pathogenesis of Epilepsy

Shimada

Takemiya

Sugiura

et al. 2014

Mediators of Inflammation

144

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Epilepsy is one of the most common chronic brain disorders worldwide, affecting 1% of people across different ages and backgrounds. Epilepsy is defined as the sporadic occurrence of spontaneous recurrent seizures. Accumulating preclinical and clinical evidence suggest that there is a positive feedback cycle between epileptogenesis and brain inflammation. Epileptic seizures increase key inflammatory mediators, which in turn cause secondary damage to the brain and increase the likelihood of recurrent seizures. Cytokines and prostaglandins are well-known inflammatory mediators in the brain, and their biosynthesis is enhanced following seizures. Such inflammatory mediators could be therapeutic targets for the development of new antiepileptic drugs. In this review, we discuss the roles of inflammatory mediators in epileptogenesis.

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“…However those authors reported rofecoxib did not reduce memory deficit and delayed neuronal death (Kunz et al, 2005). In associated with febrile seizure, the potent COX inhibitor has more disadvantage of seizure activity than weak COX inhibitor (Rantala et al, 2001). However the preventive use of ibuprofen as a safe NSAID used largely worldwide for recurrent febrile seizure was not recommended.…”

Section: Resultsmentioning

confidence: 99%

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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Systematic review of the role of prostaglandins and their synthetase inhibitors with respect to febrile seizures

Cited by 15 publications

References 34 publications

Prostaglandin F2α FP receptor antagonist improves outcomes after experimental traumatic brain injury

Prostaglandin F2α FP receptor antagonist improves outcomes after experimental traumatic brain injury

Role of Inflammatory Mediators in the Pathogenesis of Epilepsy

Effect of Phenylbutazone on Pentylenetetrazole-Induced Seizure in Mice

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