Effect and Mechanism of Epigallocatechin-3-gallate on Learning and Memory Abilities of Epileptic Rats / 中国实验方剂学杂志

ObjectiveTo investigate the effects of epigallocatechin-3-gallate （EGCG） on learning and memory abilities of amygdala electrical kindling-induced epilepsy in rats and its mechanism. MethodMale SD rats were randomly divided into the normal group， model group， intervention group （model+25 mg·kg-1 EGCG）， and EGCG group （25 mg·kg-1 EGCG）. Rats in the EGCG group were only given EGCG intraperitoneal injection， those in the normal group were only given electrode implantation， and those in the other experimental groups were given amygdala electrical kindling stimulation to establish a chronic kindling epilepsy model. EGCG was injected intraperitoneally daily before electrical stimulation. Twenty-four hours after the last electrical stimulation， the escape latency and percentage of target quadrant were recorded by the Morris water maze. Twenty-four hours after the behavioral test， rats in each group were sacrificed by decapitation. The number of hippocampal neurons was observed by Nissl staining. The thickness of postsynaptic density in the hippocampus， synaptic cleft， length of active zone and the curvature of synaptic interface were observed by transmission electron microscopy （TEM）. The expressions of synapse-related proteins synaptotagmin （Syt）， postsynaptic density-95 （PSD-95） and Kalirin-7 in the hippocampus were examined by Western blot. ResultCompared with those in the normal group， the escape latency was significantly prolonged （P<0.05， P<0.01） and the target quadrant ratio was significantly decreased in the model group （P<0.05）. The number of hippocampus neurons decreased significantly （P<0.01）. The synaptic cleft of the hippocampus was widened significantly， and the length of active zone and the thickness of postsynaptic density were significantly decreased （P<0.05， P<0.01）. The expressions of synapse-related proteins Syt， PSD-95 and Kalirin-7 in the hippocampus were significantly decreased （P<0.05，P<0.01）. Compared with those in the model group， the escape latency was significantly shortened and the percentage of target quadrant was significantly increased in the intervention group （P<0.05， P<0，01）. The number of hippocampal neurons significantly increased （P<0.01）. The synaptic cleft of the hippocampus was significantly shortened， and the length of active zone and postsynaptic density were significantly increased （P<0.05， P<0.01）. The expressions of synaptic related proteins Syt， PSD-95 and Kalirin-7 were significantly increased （P<0.05， P<0.01）. ConclusionEGCG can effectively improve cognitive dysfunction after epilepsy. Its protective effect may be achieved by protecting the ultrastructure of hippocampal synapses and regulating the expressions of synapse-related proteins Syt， PSD-95 and Kalirin-7.

The antiepileptic activity of Safranal in kindling model of epilepsy in male rats

Abstract Recent studies suggested that safranal exerts anticonvulsant properties. The present study aimed to investigate the effect of safranal on epileptic activities in the amygdala electrical kindling model in male rats. Animals were implanted with a recording electrode on the skull and a tripolar in the amygdala. After 10 days of recovery, the afterdischarge (AD) threshold of each animal was determined and stimulated once daily the AD threshold for full kindling development. Then, parameters including afterdischarge duration (ADD), stage 4 latency (S4L), stage 5 duration (S5D), and stimulation threshold were determined before and after injection of safranal (0.05, 0.1, 0.2 ml/ kg; i.p). While the dose of 0.05 ml/kg had no significant effect, the dose of 0.1 ml/kg increased the AD threshold as well as S4L and decreased the S5D (P<0.05). Injection of 0.2 ml/kg of the safranal significantly decreased the ADD and S5D (P<0.05) and 83.3% of animals had no stage 4 and stage 5 of kindling (P<0.001). Based on the obtained data safranal has anticonvulsant effects dosedependently. It seems that a dose of 0.2 ml/kg is the minimum effective dose. Further investigation is warranted to conduct the clinical implications for the treatment of epileptic disorders

Expression of P-glycoprotein in brain tissue and peripheral blood in refractory epileptic rats with amygdale kindled by electricity and kainic acid / 临床神经病学杂志

Objective To explore the possible mechanism of over expression of P-glycoprotein(Pgp) in brain tissue and peripheral blood in refractory epileptic rats with amygdale kindled by electricity and kainic acid,and compare the expression tendency of Pgp in brain tissue and peripheral blood of the different ways to establish refractory epileptic rats models.Methods The models of refractory epileptic rats were made by electrical kindling and kainic kindling in amygdale.Group A was for amygdale-electrical-kindling rats(n=12),group B was for amygdale-kainic-kindling rats(n=12),group C was implanted electrode without kindling and Carbamazepine was given by gavage(n=8),group D was injected saline in amygdale and Carbamazepine was given by gavage(n=8),group E was implanted electrode without kindling and saline was given by gavage(n=8) and group F was injected saline in amygdale and saline was given by gavage(n=8).The expression of Pgp in brain tissue and peripheral blood was detected by immunohistochemistry in each group.Results The expression of Pgp in brain tissue and peripheral blood of rats in group A and B were both much higher than those in the other groups and there were statistical differences(all P