Background: Epilepsy is a chronic neurological disorder affecting an estimated 50 million
people worldwide. Emerging evidences have accumulated over the past decades supporting
the role of inflammation in the pathogenesis of epilepsy. Curcumin is a nature-derived active
molecule demonstrating anti-inflammation efficacy. However, its effects on epilepsy and corresponding
mechanisms remain elusive.
Objective: To investigate the effects of curcumin on epilepsy and its underlying mechanism.
Method: Forty Sprague Dawley rats were divided into four groups: (1) control group; (2) Kainic
Acid (KA)-induced epilepsy group; (3) curcumin group; and (4) curcumin pretreatment before KA
stimulation group. Morris water maze was utilized to assess the effect of curcumin on KA-induced
epilepsy. The hippocampi were obtained from rats and subjected to western blot. Immunohistochemistry
was conducted to investigate the underlying mechanisms.
Results: Rats received curcumin demonstrated improvement of recognition deficiency and epilepsy
syndromes induced by KA. Western blot showed that KA stimulation increased the expression
of IL-1β and NLRP3, which were reduced by curcumin treatment. Further investigations revealed
that curcumin inhibited the activation of NLPR3/inflammasome in epilepsy and reduced
neuronal loss in hippocampus.
Conclusion: Curcumin inhibits KA-induced epileptic syndromes via suppression of NLRP3 inflammasome
activation; therefore, offers a potential therapy for epilepsy.