Curcumin Lowers the Accelerated Speed of Epileptogenesis by Traumatic Brain Injury

Authors
Hanieh Jahi 1
Mansoureh Eslami 2
Mohammad Sayyah* 3
Fariba Karimzadeh 4
Melika Alesheikh 5
1 Department of Physiology, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2 Department of Basic Sciences, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3 Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran
4 Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran
5 Department of pharmacy, Tehran University of Medical Sciences, Tehran, Iran
10.61186/ibj.3978
Abstract
Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.
Keywords
Glial fibrillary acidic protein
IL-1β
Post-traumatic epilepsy
Traumatic brain injury