摘要
目的探讨p38丝裂素活化蛋白激酶(p38 MAPK)在癫痫持续状态(SE)大鼠海马结构的活性变化规律及其意义。方法建立氯化锂-匹罗卡品(LiCL-PILO)癫痫持续状态模型,在不同时间点用免疫组化法检测海马结构p38的磷酸化状态(P-p38),并观察组织病理学改变。结果SE 30 min P-p38在各区活化程度均增高,6h后P-p38表达减弱。在所有时间点,齿状回免疫组化阳性的神经元均显著高于CA1区和CA3区,海马结构各区可见到许多神经元发生变性和坏死。结论p38 MAPK信号转导途径在匹罗卡品致痫过程中被激活,并可能参与了CA1区、CA3区癫痫后神经神经元易损性的形成。
Objective To investigate the spatiotemporal distribution pattern of active p38 in rat hippocampal formation following pilocarpine-induced status epilepsy（SE） and to discuss the significance. Methods The lithium-pilocarpine-induced model of SE was established to evaluate the phosphorylation forms of p38 （P-p38） by immunohistochemistry and histopathology changes were observed at different times after pilocarpine injection. Results In pilocarpine-treated rats, the hippocampal neurons showed a strong immunoreativity of P-p38 in the body at 30 min after pilocarpine injection, while decreased markedly at 6h. There were more immunoreactive positive cells in the dentate gyrus than those in regions of CA1 and CA3. Many injured neurons were found in hippocampus of SE rats. Conclusion p38MAPK signal transduction pathyway can be activated in SE induced by pilocapine,and may play a critical role in neurons vulnerability in regions of CA1 and CA3 after epilepsy.
出处
《重庆医学》
CAS
CSCD
2007年第13期1259-1260,共2页
Chongqing medicine
