颞叶内侧癫痫患者海马区胶质细胞中GFAP、GLAST和GLT-1的表达

Expression of GFAP,GLAST and GLT-1 in gliacytes of patients with mesial temporal lobe epilepsy

目的研究胶质纤维酸性蛋白(GFAP)及谷氨酸-胱氨酸转运体(GLAST)、神经胶质谷氨酸转运体(GLT-1)在颞叶癫痫患者海马区的表达情况。方法取40例难治性颞叶内侧癫痫患者在手术中切除的海马组织,根据在光镜下观察到的神经元丢失情况,分为海马硬化组(A组)23例和海马非硬化组(B组)17例,通过免疫组化法检测两组GFAP、GLAST、GLT-1的表达情况。结果A组GFAP的表达与B组比较,总海马区域、CA1区、CA2区、齿状回表达增加(P<0.01)。A组GLAST的表达与B组比较,海马总区域、齿状回差异无显著性(P>0.05)、CA1区减少(P<0.05)、CA2区则增加(P<0.05)。A组GLT-1的表达与B组比较,总海马区域、CA1区减少(P<0.01)、CA2区增加(P<0.01),齿状回差异无显著性(P>0.05)。结论颞叶内侧癫痫患者海马各区GFAP表达增加,GLAST、GLT-1在海马CA1区减少、CA2区表达增加,提示癫痫发作后海马区谷氨酸转运体重新分布可能是难治性癫痫发病机制之一。

Objective To determine the expression of glial fibrillary acidic protein （ GFAP）, glutamate-cystine transporter （ GLAST）, and glial glutamate transporter 1 （ GLT-1 ） in patients with mesial temporal lobe epilepy. Methods The medial temporal cortex and hippocampus from 40 patients with temporal lobe epileptogenie were harvested in surgery. The patients were classified into two groups based on the hippocampus was characterized by neuronal loss and astroglial proliferation of the surgically resected hippocampi sclerotic hippoeampus group （n = 23） and non-sclerotic hippocampus group （control, n = 17） in the hippocampal. The expression of GFAP, GLAST and GLT-1 in gliacytes in the specimens was assessed using immunohistochemical staining. Results In the specimens from sclerotic hippoeampus group, the level of GFAP in each area of the hippocampus increased significantly in comparison with the control group （ P 〈0.01 ）. The GLAST expression in the CA1 area decreased but increased significantly in the CA2 area compared with that in the control group （P 〈 0.05）. The sclerotic hippoeampus group showed decreased GLT-1 expression in the hippocampus as well as in the CA1 area but increased significantly in the CA2 area compared with the control group （P 〈 0.01 ）. Conclusions The expression of GFAP increased in various districts of the hippocampus while G1AST and GLT-1 expression decreased in the hippocampal CA1 area but increased in the CA2 area in patients with medial temoral lobe epilepsy. This suggests that the alterations of glial glutamate transporter of hippocampi after seizures may be associated with the pathogenesis of intractable epilepsy.