摘要
Background Tenidap is a liposoluble non-steroidal anti-inflammatory drug that is easily distributed in the central nervous system and also inhibits the production and activity of cyclooxygenase-2 （COX-2） and cytokines in vitro. This study aimed to evaluate the neuroprotective effect of tenidap in a pilocarpine rat model of temporal lobe epilepsy （TLE）. Methods Tenidap was administered daily at 10 mg/kg for 10 days following pilocarpine-induced status epilepticus （SE） in male Wistar rats after which prolonged generalized seizures resulted in TLE. After tenidap treatment, spontaneous recurrent seizures （SRSs） were recorded by video monitoring （for 7 hours per day for 14 days）. The frequency and severity of the SRSs were observed. Histological and immunocytochemical analyses were used to evaluate the neuroprotective effect of tenidap and detect COX-2 expression, which may be associated with neuronal death. Results There were 46.88±10.70 survival neurons in tenidap-SE group, while there were 27.60±5.18 survival neurons in saline-SE group at -2.4 mm field in the CA3 area. There were 37.75±8.78 survival neurons in tenidap-SE group, while there were 33.40±8.14 survival neurons in saline-SE group at -2.4 mm field in the CA1 area. Tenidap treatment significantly reduced neuronal damage in the CA3 area （P 〈0.05） and slightly reduced damage in the CA1 area. Tenidap markedly inhibited COX-2 expression in the hippocampus, especially in the CA3 area. Conclusion Tenidap conferred neuroprotection to the CA3 area in a pilocarpine-induced rat model of TLE by inhibiting COX-2 expression.
Background Tenidap is a liposoluble non-steroidal anti-inflammatory drug that is easily distributed in the central nervous system and also inhibits the production and activity of cyclooxygenase-2 （COX-2） and cytokines in vitro. This study aimed to evaluate the neuroprotective effect of tenidap in a pilocarpine rat model of temporal lobe epilepsy （TLE）. Methods Tenidap was administered daily at 10 mg/kg for 10 days following pilocarpine-induced status epilepticus （SE） in male Wistar rats after which prolonged generalized seizures resulted in TLE. After tenidap treatment, spontaneous recurrent seizures （SRSs） were recorded by video monitoring （for 7 hours per day for 14 days）. The frequency and severity of the SRSs were observed. Histological and immunocytochemical analyses were used to evaluate the neuroprotective effect of tenidap and detect COX-2 expression, which may be associated with neuronal death. Results There were 46.88±10.70 survival neurons in tenidap-SE group, while there were 27.60±5.18 survival neurons in saline-SE group at -2.4 mm field in the CA3 area. There were 37.75±8.78 survival neurons in tenidap-SE group, while there were 33.40±8.14 survival neurons in saline-SE group at -2.4 mm field in the CA1 area. Tenidap treatment significantly reduced neuronal damage in the CA3 area （P 〈0.05） and slightly reduced damage in the CA1 area. Tenidap markedly inhibited COX-2 expression in the hippocampus, especially in the CA3 area. Conclusion Tenidap conferred neuroprotection to the CA3 area in a pilocarpine-induced rat model of TLE by inhibiting COX-2 expression.
基金
This study was supported by a grant of National Natural Science Foundation of China （No. 81100964）.
