CONTEXT: Temporal lobe epilepsy (TLE) is an intractable neurological disorder. Curcumin is the bioactive component of turmeric with anti-epileptic and neuroprotective potential. OBJECTIVE: The beneficial effect of curcumin on the intrahippocampal kainate-induced model of TLE was investigated. MATERIALS AND METHODS: Rats were divided into sham, curcumin-pretreated sham, kainate and curcumin-pretreated kainate groups. The rat model of TLE was induced by unilateral intrahippocampal injection of 4 μg of kainate. Rats received curcumin p.o. at a dose of 100 mg/kg/d starting 1 week before the surgery. Seizure activity (SE) and oxidative stress-related markers were measured. Furthermore, the Timm index for evaluation of mossy fiber sprouting (MFS) and number of Nissl-stained neurons were quantified. RESULTS: All rats in the kainate group had SE, while 28.5% of rats showed seizures in the curcumin-pretreated kainate group. Malondialdehyde and nitrite and nitrate levels significantly increased in the kainate group (p < 0.01 and p < 0.05, respectively), and curcumin significantly lowered these parameters (p < 0.05). Superoxide dismutase activity significantly decreased in the kainate group (p < 0.05) and curcumin did not improve it. Rats in the kainate group showed a significant reduction of neurons in Cornu Ammonis 1 (CA1) (p < 0.05), CA3 (p < 0.005) and hilar (p < 0.01) regions, and curcumin significantly prevented these changes (p < 0.05-0.005). The Timm index significantly increased in the kainate group (p < 0.005), and curcumin significantly lowered this index (p < 0.01). DISCUSSION AND CONCLUSION: Curcumin pretreatment can attenuate seizures, lower some oxidative stress markers, and prevent hippocampal neuronal loss and MFS in the kainate-induced model of TLE.
CONTEXT: Temporal lobe epilepsy (TLE) is an intractable neurological disorder. Curcumin is the bioactive component of turmeric with anti-epileptic and neuroprotective potential. OBJECTIVE: The beneficial effect of curcumin on the intrahippocampal kainate-induced model of TLE was investigated. MATERIALS AND METHODS:Rats were divided into sham, curcumin-pretreated sham, kainate and curcumin-pretreated kainate groups. The rat model of TLE was induced by unilateral intrahippocampal injection of 4 μg of kainate. Rats received curcumin p.o. at a dose of 100 mg/kg/d starting 1 week before the surgery. Seizure activity (SE) and oxidative stress-related markers were measured. Furthermore, the Timm index for evaluation of mossy fiber sprouting (MFS) and number of Nissl-stained neurons were quantified. RESULTS: All rats in the kainate group had SE, while 28.5% of rats showed seizures in the curcumin-pretreated kainate group. Malondialdehyde and nitrite and nitrate levels significantly increased in the kainate group (p < 0.01 and p < 0.05, respectively), and curcumin significantly lowered these parameters (p < 0.05). Superoxide dismutase activity significantly decreased in the kainate group (p < 0.05) and curcumin did not improve it. Rats in the kainate group showed a significant reduction of neurons in Cornu Ammonis 1 (CA1) (p < 0.05), CA3 (p < 0.005) and hilar (p < 0.01) regions, and curcumin significantly prevented these changes (p < 0.05-0.005). The Timm index significantly increased in the kainate group (p < 0.005), and curcumin significantly lowered this index (p < 0.01). DISCUSSION AND CONCLUSION:Curcumin pretreatment can attenuate seizures, lower some oxidative stress markers, and prevent hippocampal neuronal loss and MFS in the kainate-induced model of TLE.