Evaluation of malondialdehyde and Tumor Necrosis Factor-alpha level in the brain of carbamazepine and vitamin B-6 combined treatment groups in the infant rat model of maximum electroshock seizure

Despite the development of new drugs over the past 20 years, the proportion of drug-resistant epilepsy has not changed. In this study, the effect of vitamin B6 and carbamazepine cotreatment was investigated on the duration of the tonic response, the malondialdehyde (MDA) and tumor necrosis factor alpha (TNF-α) levels in the brain of neonate rats in the maximal electroshock (MES) model.

Seventy neonatal Wistar rats were divided into seven groups: (1) control, (2) saline and MES, (3) carbamazepine (40 mg/kg), (4 and 5) vitamin B-6 (300 and 600 mg/kg), and (6 and 7) vitamin B-6 + carbamazepine (300 + 40 mg/kg) and (600 + 40 mg/kg). All drugs were injected intraperitoneally 1 hour before applying MES. The duration of hind leg extension (HLE), and the level MDA and TNF-α in brain homogenate of rats were measured.

The treatments did not affect the number of deaths of rats. Administration of carbamazepine (40mg/kg, i.p.) and vitamin B6 (300 mg/kg, i.p.) significantly (p <0.01) reduced the HLE duration. Vitamin B-6 (600 mg/kg) only enhanced the reducing effect of carbamazepine on the duration of HLE compared to the carbamazepine alone group. Treatment with vitamin B-6 and carbamazepine alone reduced the level of MDA and TNF-α in the brain of convulsive rats, but their combined administration did not have a synergistic effect on the suppression of these factors.

The mechanism underlying the enhancement of the anticonvulsant response of carbamazepine administration with vitamin B-6 is independent of the modulation of MDA and TNF-a in the brain.