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• W164219356 startingPage "145" @default.
• W164219356 abstract "The CNS inflammatory reaction occurring after aneurysmal subarachnoid hemorrhage (SAH) involves the upregulation of numerous cytokines and prostaglandins. Cyclooxygenase (COX) inhibition is a well-established pharmacological anti-inflammatory agent. Previous studies have shown marked increases in COX-2 expression in neurons, astrocytes, microglia, and endothelial cells following brain injury. COX-2 inhibition has been shown to be beneficial following various types of brain injury. This experiment investigates the role of COX-2 activity in early brain injury following SAH. CD-1 mice were subjected to an endovascular perforation model of SAH or SHAM surgery. Following experimental SAH animals were treated with the specific COX-2 inhibitor, NS398, in dosages of either 10 or 30 mg/kg. Neurological performance and brain edema were evaluated 24 and 72 h after SAH. NS398 at 30 mg/kg significantly reduced SAH-induced neurological deterioration. NS 398 at 30 mg/kg resulted in a trend toward the reduction of SAH-induced cerebral edema. Treatment had no effect on mortality. This experiment provides preliminary evidence that COX-2 inhibition is an effective pharmacological intervention for the prevention of brain edema and the preservation of neurological function following SAH." @default.
• W164219356 created "2016-06-24" @default.
• W164219356 creator A5008223461 @default.
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• W164219356 date "2011-01-01" @default.
• W164219356 modified "2023-09-24" @default.
• W164219356 title "The Neuroprotective Effects of Cyclooxygenase-2 Inhibition in a Mouse Model of Aneurysmal Subarachnoid Hemorrhage" @default.
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• W164219356 doi "https://doi.org/10.1007/978-3-7091-0693-8_24" @default.
• W164219356 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21725746" @default.
• W164219356 hasPublicationYear "2011" @default.
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