作者: R. Ayer , V. Jadhav , T. Sugawara , John H. Zhang
DOI: 10.1007/978-3-7091-0693-8_24
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摘要: 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 neurons, astrocytes, microglia, endothelial cells following brain injury. has been to be beneficial various types This experiment investigates role activity early injury SAH. CD-1 mice were subjected an endovascular perforation model SAH or SHAM surgery. Following experimental animals treated with specific inhibitor, NS398, dosages either 10 30 mg/kg. Neurological performance edema evaluated 24 72 h NS398 at mg/kg significantly reduced SAH-induced neurological deterioration. NS 398 resulted trend toward reduction cerebral edema. Treatment had no effect on mortality. provides preliminary evidence that effective intervention for prevention preservation function