Abstract of research

Biochemical role of curcumin on kainic acid-induced epilepsy in male swiss albino mice

Samy Ali Hussein; Afaf D. Abdel-mageid; Omnia M. Abd-Elhamed and Hassan S. Al-Harthy

Abstract

Oxidative stress resulting from excessive free-radical release is likely implicated in the initiation and progression of epilepsy. The potential protective and treatment effect of curcumin (CUR) administration on KA-induced epilepsy in mice was evaluated. Twenty-four male Swiss Albino mice were divided into four groups. Group Ι:(Control group) mice received no drugs. Group Π:(epilepsy-induced group): mice administered with a single dose of KA (10 mg/kg b.wt) intraperitoneally (i.p). Group III:(epilepsy+ CUR protected group) mice received CUR (200 mg/kg b.wt/day/orally) for 7 days before KA administration. Group IV:(epilepsy+ CUR treated group): mice first injected with KA(10 mg/kg b.wt/i.p.) then after 15 min. CUR was administered as in group III for 3 consecutive days. Blood samples and brain tissue specimens were collected after 12 hours and 3 days from the onset of KA administration for determination of serum sialic acid (SA) and tumor necrosis factor alpha (TNF-α), brain tissue superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), reduced glutathione (GSH), LMalondialdehyde (L-MDA), nitric oxide (NO), caspase-3 and DNA-fragmentation. The obtained results showed that, KA-induced epilepsy in mice caused significant decrease in serum SA, and brain tissue SOD, CAT, GPX activities and GSH concentration. However, serum TNF-α and brain tissue NO, LMDA levels, caspase-3 activity and DNA-fragmentation were significantly increased. Administration of CUR was able to mitigate KA- induced epilepsy through rising of serum SA and brain tissue SOD, CAT, GPX activities and GSH in addition to declining NO, L-MDA, caspase-3 and DNA-fragmentation in brain tissue. These results suggest that, CUR may be successful in the treatment of epilepsy by its radical scavenging, anti-inflammatory and antiapoptotic activities and regenerating endogenous antioxidant mechanism. In addition, curcumin protects mice brain against KA induced neuronal damage, decrease the severity of epilepsy and attenuated kainite induced inflammation and apoptosis.