Curcumin Lowers the Accelerated Speed of Epileptogenesis by Traumatic Brain Injury

Iran Biomed J. 2024 Mar 1;28(2&3):113-9. doi: 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.

MeSH terms

  • Animals
  • Brain Injuries, Traumatic* / complications
  • Brain Injuries, Traumatic* / drug therapy
  • Curcumin* / pharmacology
  • Curcumin* / therapeutic use
  • Epilepsy* / drug therapy
  • Glial Fibrillary Acidic Protein* / metabolism
  • Hippocampus* / drug effects
  • Hippocampus* / metabolism
  • Interleukin-1beta* / metabolism
  • Kindling, Neurologic* / drug effects
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Seizures / drug therapy

Substances

  • Curcumin
  • Interleukin-1beta
  • Glial Fibrillary Acidic Protein