Does inhibition of the NLRP3 inflammasome provide neuroprotection in rats following amygdala kindling-induced status epilepticus?
Our study provides the first evidence that the NLRP3 inflammasome was significantly up-regulated following SE. More importantly, we show that inhibition of the NLRP3 inflammasome provides neuroprotection in rats following SE. These findings suggest that NLRP3 may represent a potential target for the treatment of epileptogenesis.
Our results indicated the disrupted topological properties of whole brain functional networks in TLE patients.