摘要
目的观察其海马经HE染色后组织病理学、胶质纤维酸性蛋白免疫反应阳性表达细胞在LPS中各观察时间点海马CA1、CA3、齿状回的表达,探讨其致机制。方法锂-匹罗卡品急性诱导SD癫持续状态模型鼠形成后,采用免疫组化和图像分析方法观察海马HE染色组织病理学、胶质纤维酸性蛋白免疫反应阳性表达细胞。结果模型组各时间点海马细胞形态出现病理性改变,部分细胞脱失,胞浆浓缩,胞核固缩深染;胶质纤维酸性蛋白免疫反应阳性表达细胞亦显著上调(P<0.05)。结论Pilo诱导SD大鼠癫发作后存在显著的海马神经元结构和胶质细胞的损伤,以胶质细胞损伤更显著,胶质纤维酸性蛋白持续高表达可能是这种功能异常的胶质细胞增生的重要原因,也可能是锂-匹罗卡品致癫发作的重要因素之一。
Objective To observe the expression of histopathology, the positive cells in the glial fibrillary acidic protein （GFAP） immunoreactivity （IR） （GFAP-IR） in the CA1, CA3, and Dentate Gyrus （DG） areas at different time-point, and explore the epileptogenesis in the LPS model. Methods After the acute status epileticus by using pilocarpine, observing the HIP histopathology and the positive cells （PC） were observed with the image analysis and the immunohistochemistry respectively. Results The nerve cells were disarranged with morphocytology pathological change, part of cell loss, cytoplasm eoneentration, nuclei condensation and hyperchromatosis in the model group. There were lots of GFAP IR positive cells in the HIP pyramidal layer and the dentate band granular cell layer. GFAP-IR positive cells increased significantly in the model group compared with the control group （P〈0. 05）. Conclusions There were obvious LPS rats＇ hippocampus neuron structure and astrocyte damage, GFAP＇s continuous high expression may be the important cause to the astrocyte hyperplasia appearance which functions exceptionally, as well as one factor of the LPS epilepsy outbreaks repeatedly.
出处
《卒中与神经疾病》
2009年第5期280-283,共4页
Stroke and Nervous Diseases
基金
四川省攻关课题立项资助(05SG1672)
四川省中医药管理局立项资助(20060068)
