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Aim:To examine whether the prostaglandins(PGs)pathway is involved in trigger-ing delayed neuroprotection by ischemic preconditioning(IPC)and evaluate theeffects of IPC on cyclooxygenase-2(COX-2)expression following focal cerebralischemia and reperfusion in rats.Methods:IPC was induced by 10 min of salineinfusion into the left internal carotid artery with the right common carotid arteryclamped at the same time.Middle cerebral artery occlusion(MCAO)and reperfusionmodel was produced using intraluminal filament method.Results:IPC 48 h priorto MCAO significantly reduced infarct area as compared with MCAO alone.Anonselective inhibitor of COX indomethacin(3 mg/kg ip)applied 1 h prior to or 1 hafter IPC failed to affect its protective effects.IPC had no direct effect on thecortex COX-2 mRNA and protein expression 72 h later,but decreased the expres-sion of COX-2 mRNA and protein following ischemia and reperfusion insult.Conclusion:PGs pathways was not involved in triggering delayed neuroprotectionby IPC,and IPC induced down-regulation of COX-2 following focal cerebral is-chemia and reperfusion in rats in vivo.
Aim: To examine whether the prostaglandins (PGs) pathway is involved in trigger-ing delayed neuroprotection by ischemic preconditioning (IPC) and evaluate the effects of IPC on cyclooxygenase-2 (COX-2) expression following focal cerebral ischemia and reperfusion in rats. Methods: IPC was induced by 10 min of salineinfusion into the left internal carotid artery with the right common carotid arteryclamped at the same time .Method cerebral artery occlusion (MCAO) and reperfusion model was produced using infarct area as compared with MCAO alone. Nonselective inhibitor of COX indomethacin (3 mg / kg ip) applied 1 h prior to or 1 hafter IPC failed to affect its protective effects. IPC had no direct effect on the cortex COX-2 mRNA and protein expression 72 h later, but decreased the expres-sion of COX-2 mRNA and protein following ischemia and reperfusion insult. Conflux: PGs pathways was not involved in triggering delayed neuroprotec tion by IPC, and IPC induced down-regulation of COX-2 following focal cerebral is-chemia and reperfusion in rats in vivo.