The Effect of Oral Nanocurcumin on Intraperitoneal Pentylenetetrazole-Induced Convulsion and CaMKII Phosphorylation Pattern in the Hippocampus of Male Mice

Previous studies have shown that converting curcumin into nanoparticles can enhance its therapeutic effect in models of convulsion. Changes in calmodulin-dependent Ca2+/protein kinase (CaMKII) are associated with some experimental models of epilepsy. This study aimed to evaluate the hippocampal CaMKII phosphorylation following the therapeutic effect of nanocurcumin in a model of pentylenetetrazole (PTZ)-induced convulsion.

Nanocurcumin (with an average particle diameter of 150 nm) was produced using bovine serum albumin and was administered orally (gavage) to male NMRI mice weighing 25-30 g at doses of 50 and 100 mg/kg. One hour later, PTZ at a dose of 85 mg/kg was administered intraperitoneally to the animal. Following intraperitoneal PTZ injection, the latency of myoclonus, clonus, general tonic convulsion, and mortality rate were recorded in male mice. After behavioral testing, the anesthetized animals were euthanized, and the levels of phosphorylated and total forms of hippocampal CaMKII were determined by Western blotting technique.

The results showed that oral administration of nanocurcumin at doses of 50 and 100 mg/kg significantly improved convulsion induced by PTZ compared with natural curcumin. In all groups, convulsion increased hippocampal CaMKII phosphorylation, and nanocurcumin did not modulate it.

The findings of this study showed that the therapeutic effect of nanocurcumin in a model of pentylenetetrazole-induced convulsion was not associated with a change in hippocampal CaMKII activity pattern.