GFAP、GLAST及GLT-1在颞叶内侧癫痫患者海马胶质细胞中的表达

Expression of GFAP, GLAST, GLT-1 in gliacyte in human mesial temporal lobe epilepsy

目的：探讨胶质纤维酸性蛋白（GFAP）、谷氨酸／天冬氨酸转运体（GLAST）及谷氨酸转运体1（GLT-1）在颞叶内侧癫痫患者海马胶质细胞中的表达。方珐：选取本院神经外科住院进行前颞叶切除手术治疗的颞叶内侧癫痫患者62例作为研究对象，根据切除的海马组织在光镜下的情况分为海马硬化组、海马非硬化纽，检测两组GFAP、GLAST及GLT～1并进行比较。结果：GFAP主要表达在胶质细胞的细胞浆和突出部分，在光镜下表现为星状、蜘蛛状，海马硬化组比海马非硬化组更亮，反应性星形细胞增生肥大，并交织成网状，海马硬化组的GFAP在总海马区、CA1区、CA2区、齿状回表达均高于海马非硬化组，差异具有统计学意义（P〈0．05）；GLAsT主要表达在胶质细胞的细胞浆和细胞膜上，海马各区均可见，光镜下CA1区呈现补丁状或斑片状，海马硬化纽GLAsT在CA1区表达减少，而在CA2区表达增多，在齿状回GLAST丢失高于海马非硬化纽，差异具有统计学意义（P〈0．05）；GI，T～1主要表达在胶质细胞的细胞膜上，海马硬化组在CA2区椎体神经元之间的GLT-1表达增强，形成了椎体细胞层的“网格”，而海马硬化组在CA1区GLT—1丢失高于海马非硬化组，差异具有统计学意义（P〈0．05）。结论：癫痫频繁发作后海马胶质细胞反应性过度增生、GLAST及GI．T-1的重新分布可能是颞叶内侧癫痫发病的重要原因。

Objective： To explore the expression levels of GFAP, GLAST, GLT-1 in gliacyte in human mesiM temporal lobe epilepsy. Methods; A total of 62 patients with temporal lobe epilepsy who were treated by anterior temporal lobe resection in the Department of Neurosurgery of our hospital were enrolled as the research objects. According to the results under light microscope, these patients were divided into hippocampus sclerosis group and non-hippocampus sclerosis group. Then GLT-I of the two groups were detected and compared. Results：GFAP mainly expressed in the cytoplasm and prominent part of the glial cells and were presented as the shape of stars or spiders, which were brighter in the hippocampus sclerosis group than that in the nonhippocampus sclerosis group （P〈0.05） under the light microscope. GLAST was expressed mainly in the cytoplasm and cell membrane of glial cells. Under light microscope, the CA1 region of the hippocampus was presented as patches in different size. For the hippocampus sclerosis group, the expression of GLAST was decreased in the CA1 region while increased in CA2 region~ In the fascia dentate, the loss of GLAST was more than that of the non- hippocampus sclerosis group （P^0.05）. GLT-1 was expressed mainly in the cell membrane of glial cells. The expression of GLT-1 in the hippocampus of the CA2 region of the hippocampus sclerosis group was increased and presented as a grid. While the loss of GLT-1 in CA1 region of the hippocampus sclerosis group was more than that of the non-hippocampus sclerosis group （P^0.05）. Conclusion：The re-distri- bution of reactive proliferation of glial ceils and the re-distribution of glutamate transporters may be important factors in the pathogenesis of temporal lobe epilepsy.