Curcumin Lowers the Accelerated Speed of Epileptogenesis by Traumatic Brain Injury

Traumatic brain injury or TBI can underlie epilepsy. Prevention of PTE has been of great interest to scientists. Given the antiepileptic, antioxidant and anti-inflammatory activities of curcumin, we examined whether this compound can affect epileptogenesis in rats after TBI.

Curcumin was injected once a day for two weeks. TBI was induced in the temporal cortex of anesthetized rats using a controlled cortical impact device. One day after TBI, pentylenetetrazole (PTZ), 35 mg/kg, was injected i.p. every other day until manifestation of generalized seizures. The number of PTZ injections was then recorded. Moreover, the extent of cortical and hippocampal IL-1β and glial fibrillary acidic protein (GFAP) expression in the epileptic rats were measured by Western blot analysis.

Curcumin 50 and 150 mg/kg prevented the development of kindling, whereas TBI accelerated the rate of kindling. Curcumin 20 mg/kg prohibited kindling facilitation by TBI, and reduced the expression of IL-1β and GFAP induced by TBI.

Curcumin can stop the acceleration of epileptogenesis after TBI in rats. Inhibiting hippocampal and cortical overexpression of IL-1β and GFAP seems to be involved in this activity.