The present study was undertaken to evaluate the potential protective and therapeutic effect of curcumin (CUR) administration on KA-induced epilepsy in rats. Twinty four male albino rats were divided into four groups. Group Ι :(Control group): received no drugs. Group Π :( epilepsy non-treated group): administered with a single injected dose of 0.5 ml/rat of absolute KA for epilepsy induction. Group III :( CUR + epilepsy, protected group): received CUR (200 mg/kg body weight/day) orally for 7 days before KA administration. Group IV :(epilepsy + CUR, treated group) received CUR as in group III and the treatment was continued for 3 days later.
Blood samples for serum separation and brain tissue were collected at the 12 hours and 3 days. days from the onset of CUR administration for determination of serum sialic acid (SA) and TNFalpha, brain tissue Superoxide dismutase (SOD), Catalase (CAT) and Glutathione peroxidase (GPx), , , reduced glutathione (GSH), L- Malondialdehyde (L-MDA), nitric oxide (NO), caspase-3 and DNA-fragmentation . The obtained results showed that, KA induced epilepsy caused a significant decrease in serum SA, and brain tissue SOD, CAT, GPX, , GSH activities. However, , TNFalpha, NO L-MDA, caspase-3 and DNA-fragmentation were significantly increased. Administration of CUR was able to mitigate epilepsy induced by KA through increasing of SA, and brain tissue SOD, CAT, GPX, , GSH activities in addition to decreasing NO, L-MDA, caspase-3 and DNA-fragmentation in brain tissue. These results suggest that, CUR may be successful in the therapeutic of brain epilepsy by its radical scavenging and antiapoptotic activity, inhibited neutrophil accumulation and regenerating endogenous antioxidant mechanisms. Curcumin protects rat brain against KA induced neuronal damage through modulation of MDA, GPx, SOD and CAT activities, reduced the level of NO. Also, curcumin decrease the severity of epilepsy, attenuated kainite induced inflammation and apoptosis
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