Aspirin attenuates spontaneous recurrent seizures and inhibits hippocampal neuronal loss, mossy fiber sprouting and aberrant neurogenesis following pilocarpine-induced status epilepticus in rats.

Accumulating data suggest that inflammation may contribute to epileptogenesis in experimental models as well as in humans. However, whether anti-inflammatory treatments can prevent epileptogenesis still remains controversial. Here, we examined the anti-epileptogenic effect and possible mechanisms of aspirin, a non-selective Cyclooxygenase (COX) inhibitor, in a rat model of lithium-pilocarpine-induced status epilepticus (SE). Epileptic rats were treated with aspirin (20mg/kg) at 0h, 3h, or 24h after the termination of SE, followed by once daily treatment for the subsequent 20 days. We found that aspirin treatment significantly reduced the frequency and duration of spontaneous recurrent seizures during the chronic epileptic phase. Hippocampal neuronal loss five weeks after SE was also attenuated in the CA1, CA3 and hilus following aspirin administration. Furthermore, the aberrant migration of newly generated granule cells and the formation of hilar basal dendrites were prevented by aspirin. Treatment with aspirin starting at 3h or 24h after SE also suppressed the development of mossy fiber sprouting. These findings suggest the possibility of a relative broad time-window for aspirin intervention in the epileptogenic process after injury. Aspirin may serve as a potential adjunctive therapy for individuals susceptible to chronic epilepsy.