查看文章

The intracellular calcium overload resulting from glutamate excitotoxicity is considered major determinant for neuronal loss during cerebral ischemia. Moreover, acidosis mediated ASIC1a activation has also shown to promote intracellular calcium overload following ischemic insult. Interestingly, ASIC1a was found to be inhibited by NSAIDs particularly flurbiprofen and ibuprofen, which could be exploited in hypoxic conditions like cerebral ischemia. This prompted us to investigate neuroprotective effect of flurbiprofen, besides its possible downstream signaling mechanism in rodent model of focal cerebral ischemia. The flurbiprofen treatment, 30 min prior to ischemia and 4 h post-reperfusion, afforded significant neuroprotection from ischemic injury as evidenced by reduction in cerebral infarct volume and neurobehavioral deficit. Further, an early calcium dependant rise in levels of nitrite and MDA was also found to be …