癫痫杂志

癫痫杂志

难治性癫痫致痫灶 EPO-R、JAK2 和 STAT-5 的表达及分析

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目的 明确难治性癫痫致痫灶中 EPO-R、JAK2 和 STAT-5 的表达情况,并探讨 EPO-R/JAK2/STAT-5 通路与难治性癫痫致痫灶神经细胞凋亡的关系。 方法 收集 2016 年 3 月−2017 年 7 月期间于吉林大学第一医院癫痫中心住院并行手术治疗的难治性癫痫患者脑组织 24 例(试验组)和同期长春市因意外死亡或非自然死亡后按有关法律规定立即进行尸体解剖所取得的对照组脑组织 6 例,应用免疫组织化学技术,观察上述两组脑组织 EPO-R、JAK2 和 STAT-5 的表达差异并进行统计学分析。 结果 ① 试验组与对照组脑组织中均有 EPO-R、JAK2 和 STAT-5 表达,400 倍光镜下试验组 EPO-R、JAK2 和 STAT-5 的阳性细胞数分别为 41.05±2.40、50.21±2.50、60.18±2.84;对照组分别为 23.00±0.49、27.00±0.88、25.93±0.33。试验组与对照组差异明显,具有统计学意义(P<0.001);② 试验组患者致痫灶病理及超微结构变化:在光镜下可见神经元分布不均,不成熟神经元;细胞核呈空泡状,胞质少,深染,胞浆嗜酸小体,神经元变性呈三角形;还可见胶质细胞及小血管增生,嗜神经细胞现象;电镜下致痫灶可见神经细胞变性坏死,核固缩变形,核仁偏位,核膜断裂甚至溶解;星形胶质细胞肿胀,染色质边集,细胞膜水肿扩充;线粒体肿胀透明,部分线粒体空泡化,嵴异常。 结论 ① 难治性癫痫致痫灶中可见神经细胞凋亡;② 难治性癫痫致痫灶中 EPO-R、JAK2 和 STAT-5 在神经元细胞及神经胶质细胞表达均较对照组明显增加,EPO-R、JAK2 和 STAT-5 的高表达与癫痫病程及发作频率无相关性;③ EPO-R/JAK2/STAT-5 通路可能参与了癫痫发作后内源性 EPO 保护神经细胞的病理生理过程。

Objective The purpose of this study was to explore the expressions of EPO-R, JAK2 and STAT-5 in the human brain with refractory epilepsy and the role in neural apotosis. Methods Collecting the brain tissue of 24 patients with intractable epilepsy (as experimental group) who were hospitalized and underwent surgery in the Epilepsy Center of the First Hospital Jilin University between March 2010 to July 2011 and 6 cases of accidental or unnatural death immediately following autopsy (as control group) as required by law during the same term. Immunohistochemical was performed to observe the expression of EPO-R, JAK2 and STAT-5 in brain tissue and statistical analysis was performed. Results ① EPO-R, JAK2 and STAT-5 were expressed in both experimental and control groups. In experimental group, the positive-cell number were 41.05±2.40, 50.21±2.50 and 60.18±2.84 under light microscope (400×). While in control group, the positive-cell number were 23.00±0.49, 27.00±0.88 and 25.93±0.33. There were significant differences between the 2 groups (P<0.001). ② There were the pathologic and ultrastructural changes in the human brain with refractory epilepsy. Under the optical microscope, we can observe that the distribution of neurons was uneven and immature neurons were visible. We can see that the nuclei were vacuolar, less cytoplasm, dark staining, hyalomitome acidophilic body, and the neurons became triangular due to degeneration. The proliferation and hyperemia appeared in small vascular and glial cells. Under the transmission electron microscope we observed degeneration and necrosis of the nerve cells, nuclear karyopyknosis, nucleolis dyssymmetry and karyolemma breakage and even dissolution. The mitochondria and astrocytes were swelling. We also saw that part of the mitochondrial cristae was abnormal. Conclusion ① We found neuronal apotosis in the human brain with refractory epilepsy. ② The expression of EPO-R, JAK2 and STAT-5 in intractable epilepsy was significantly increased in neurons and glial cells compared with the control group. The high expression of EPO-R, JAK2 and STAT-5 is unrelated with course and frequency of epileptic seizures. ③ The pathway of EPO-R/JAK2/STAT-5 may be involved in the pathophysiological processes of neural protective effect of endogenous EPO against brain injury induced by epileptic seizures.

关键词: 难治性癫痫; 凋亡; EPO-R; JAK2; STAT-5

Key words: Intractable epilepsy; Apotosis; EPO-R; JAK2; STAT-5

引用本文: 王广文, 王赞, 林卫红, 张文娟. 难治性癫痫致痫灶 EPO-R、JAK2 和 STAT-5 的表达及分析. 癫痫杂志, 2018, 4(6): 480-485. doi: 10.7507/2096-0247.20180077 复制

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