Abstract:
:Epilepsy is one of the most common neurological diseases. It adversely affects cognitive function. Neuroinflammation has been widely recognized as an important factor involved in the pathophysiology of epilepsy. Cyclooxygenase (COX) is a type of oxidoreductase enzyme that acts in the metabolic pathway converting arachidonic acid to prostaglandins, which mediate inflammatory reactions. The activation of inducible cyclooxygenase-2 (COX-2) is considered to be a precipitating factor of neuroinflammation in the brain. Neuroinflammatory processes in the brain are known to contribute to the cascade of events leading to neuronal injury, which may consequently cause cognitive decline. Here in this study, we showed that pentylenetetrazole (PTZ)-kindled mice exhibited an increased level of COX-2 and its main product prostaglandin E2 (PGE2) along with neuroinflammation and neuronal injury in the hippocampus. Pharmacological inhibition of COX-2 by celecoxib, however, significantly reduced hippocampal neuroinflammation and neuronal injury. Furthermore, inhibition of COX-2 by celecoxib attenuated cognitive impairment in the PTZ-kindled mice, suggesting that COX-2-PGE2 signaling pathway mediated neuroinflammation and neuronal injury contributes to cognitive dysfunction in the PTZ-kindled epilepsy mice. Targeting COX-2-PGE2 signaling pathway in the epileptic brain appears to be a viable strategy for attenuating neuronal injury and preventing cognitive deficits in epilepsy patients.
journal_name
Int Immunopharmacoljournal_title
International immunopharmacologyauthors
Zhu X,Yao Y,Yang J,Zhengxie J,Li X,Hu S,Zhang A,Dong J,Zhang C,Gan Gdoi
10.1016/j.intimp.2020.106801subject
Has Abstractpub_date
2020-10-01 00:00:00pages
106801eissn
1567-5769issn
1878-1705pii
S1567-5769(20)31765-3journal_volume
87pub_type
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