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Although several animal studies have indicated the antiepileptic effect for curcumin, there are reports stating the null antiepileptic effect of this substance. This inconsistency might be due to the low bioavailability of curcumin. Therefore, the current study aimed to assess the effect of oral bovine serum albumin (BSA)-based nanocurcumin on seizure caused by pentylenetetrazol (PTZ) in mice. Furthermore, due to the suggested involvement of JNK signaling in seizure pathology, the hippocampal pattern of JNK phosphorylation (activation) was evaluated. Methods: BSA based nanocurcumin was administered at doses of 50 and 100mg/kg oral gavage to male NMRI mice, one hour before PTZ administration. Intravenous PTZ paradigm was used to determine the threshold dose of PTZ to induce clonic seizures, while the intraperitoneal PTZ paradigm was applied to evaluate the latency for appearance of generalized clonus. Upon completion of intraperitoneal PTZ paradigm experiments, the hippocampi were removed and Western blot analysis was performed to determine the phosphorylated and total forms of JNK. Results: The results indicated that BSA-based nanocurcumin at the doses of 50 and 100mg/kg could significantly increase the threshold and latency of clonic seizure, which was a significant superior effect compared to natural curcumin. PTZ significantly increased the level of hippocampal JNK phosphorylation, but pretreatment of nanocurcumin did not modify this effect. Conclusion: The present study shows that converting curcumin to BSA-based nanocurcumin can increase its antiepileptic effect. Furthermore, the antiepileptic effect of nanocurcumin was not associated with a modification in PTZ-induced hippocampal JNK hyper activation.

Anticonvulsant effect of acute curcumin nanoparticle on pentylenetetrazole-induced seizures in mice: non-involvement of JNK restoration