RESUMEN
Objective To investigate the changes of cannabinoid 2 receptor(CB2R) expression at different time after epileptic status in epileptic childhood rats. Methods Healthy male SD rats (18-21 days old) were randomly divided into two groups:control group and epileptic model group. CB2R concentration in hippocampus of rats were tested at 2 h,24 h,14 d,21 d after entering the status epilepticus( status epilepsy, SE) by immunohistochemistry,PCR,Western blot. Results In control group,CB2R content of the hippo-campus brain gradually increased with age increasing. When the rats with the age of 35-42 days,CB2R con-tent gradually got stabilized. After status epilepticus for 2 h-14 d,CB2R content of hippocampus in epileptic model group was more than that in the control group. At the point of 21 d,CB2R content of hippocampus in the control group was more than that in epileptic model group. CB2R mRNA of epileptic model group at 2 hours point was more than that of control group (2. 062 vs 1. 878,P<0. 05). At 24 h and 14 d after SE,there were significant differences between two groups in CB2R mRNA respectively ( P <0. 05, respectively). At 21 d after SE,CB2R mRNA of control group was more than that of epileptic group (6. 018 vs 5. 938),but there was no significant difference between two groups (P >0.05). Conclusion CB2R presents high expression in childhood rat hippocampus suffering from status epilepticus, reaches a peak following with prolonged seizures,then gradually decreased.
RESUMEN
Objective To explore the protective effect and probable mechanism of JNK inhibitor SP600125 on hippocampal neurons in rats with status epilepsy following lithium?pilocarpine. Methods 48 Wistar rats,in accordance with the random number table,were divided into control,status epilepticus ( SE) and JNK in?hibitor SP600125 group ( SP ) . HE staining and fluorescent TUNEL method were used to observe pathological changes and neuronal apoptosis in the hippocampal area of rats in each group. Western blot was applied to detect the phosphorylation expression of JNK and its downstream effector molecule c?JUN in hippocampal tissues of rats in each group. Results Compared with control group,neuronal loss and apoptosis in CA3 area of hippocampus in SE group were significant (percentage of TUNEL positive cells (26.34±3.04)%, P<0.05). The mortality of rats was significantly decreased and neuronal loss and apoptosis were obviously reduced in SP group than in SE group ( mor?tality in SP and SE group :6.25%,37.5% respectively, P<0.05). Meanwhile,the expression levels of phospho?JNK and phospho?c?JUN were significantly increased in hippocampus of rats in SE group ( The relative OD values respectively 0.447±0.025,0.552±0.035, P<0.05 compared with Control group). After treated with SP600125 in SP group,the phosphorylation levels of JNK and c?JUN were obviously decreased ( The relative OD values respec?tively 0.211±0.016,0.237±0.028, P<0.05 compared with SE group). Conclusion JNK inhibitor SP600125 may play an important protective effect on neurons in the rat hippocampus after status epilepticus through inhibition of JNK and c?JUN phosphorylation.