Capsaicin prevents kainic acid-induced epileptogenesis in mice

Epilepsy is a neurodegenerative disease with periodic occurrences of spontaneous seizures as the main symptom. The aim of this study was to investigate the neuroprotective effects of capsaicin, the major ingredient of hot peppers, in a kainic acid (KA)-induced status epilepticus model. After intraperitoneal injections of MA (30 mg/kg) in 8-week-old male ICR mice, the animals were treated subcutaneously with capsaicin (033 mg/kg or 1 mg/kg) and then examined for any anti-ictogenic, hypothermic, antioxidative, anti-inflammatory, and anti-apoptotic effects of the capsaicin treatment 3 days after KA treatment. MA injections significantly enhanced neurodegenerative conditions but co-injection with capsaicin reduced the detrimental effects of KA in a dose-dependent manner in mice. The co-administered group that received MA and 1 mg/kg of capsaicin showed significantly decreased behavioral seizure activity and body temperature for 3 h and also remarkably blocked intense and high-frequency seizure discharges in the parietal cortex for 3 days compared with those that received MA alone. Capsaicin treatment significantly diminished the levels of oxidant activity and malondialdehyde concentration and increased the antioxidant activity in the blood and brain of MA-treated mice. In addition, capsaicin significantly lowered the KA-induced increase in the concentration of the cytokines IL-1 beta and TNF-alpha in the brain. Furthermore, co-treatment of MA and capsaicin (1 mg/kg) resulted in considerably decreased apoptotic cell death in the cornu ammonis sections of the hippocampus compared with that seen in the KA-alone group. These findings indicate that capsaicin is preventative for the epileptogenesis induced by KA in mice. (C) 2011 Elsevier Ltd. All rights reserved.