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AKT/HIF/VEGF信号通路与p-NMDAR2B在难治性癫痫相关性FCD致痫灶中的作用及相关因素分析 被引量:1

The Significance and Relativity Analysis of AKT/HIF/VEGF Signal Path and p-NMDAR2B in the Epileptogenic Zone of the Focal Cortical Dysplasias Relative Intractable Epilepsy
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摘要 目的研究AKT/HIF/VEGF信号通路与p-NMDAR2B在难治性癫痫相关性FCD致痫灶中的作用及相关因素分析,探讨两者在FCD致痫灶中的作用及相关因素分析。方法该研究于2010年1月—2015年1月间方便选取在福建医科大学附属第一医院神经外科进行手术治疗的50例难治性癫痫患者,所有患者均经术后病理证实为FCD,将术后病灶脑组织进行研究分析,作为实验组;其中FCDⅠ型30例,FCDⅡ型20例。同时另外选取50例行减压或清创手术的脑外伤患者,将术中获取的和各种病变患者手术入路不可避免要切除的正常脑组织进行研究,纳入对照组。均利用免疫组织化学染色和Western blot方法检测上述脑组织中的p-AKT1/2/3(Thr308)、HIF-1、VEGF以及p-NMDAR2B(Tyr1336)的表达情况和蛋白水平。观察各型癫痫患者和正常脑组织p-AKT1/2/3(Thr308)、HIF-1、VEGF以及pNMDAR2B(Tyr1336)的表达情况、免疫组化积分情况以及β-actin灰度比值情况。结果 (1)各型难治性癫痫相关性FCD致痫灶中AKT/HIF/VEGF信号通路发生不同程度激活表现,属异常现象。(2)Western blot:p-AKT1/2/3(Thr308)、HIF-1、VEGF以及p-NMDAR2B(Tyr1336)在FCDⅠ型病灶中表达水平分别为(0.619 3±0.078 4)、(0.779 2±0.039 1)、(0.752 8±0.099 4)以及(0.641 4±0.091 9);在FCDⅡ型病灶中表达水平分别为(0.885 9±0.031 1)、(0.862 9±0.035 5)、(0.839 2±0.038 1)以及(0.908 8±0.037 3),均明显高于正常脑组织的(0.404 2±0.084 9)、(0.467 9±0.013 8)、(0.479 8±0.045 1)以及(0.349 2±0.090 7),差异有统计学意义(P<0.05)。结论 AKT/HIF/VEGF信号通路可能是通过调控NMDA受体活性参与了FCD相关难治性癫痫的发生发展。 Objective This paper tries to investigate the role and correlation of AKT/H IF/VEGF signaling pathway and p-N M D A R2B in refractory epilepsy-related F C D-induced epileptic foci,and to explore the role and correlation of AKT/H IF/VEGF signaling pathway in F C D-induced epileptic foci.Methods In this study,50 patients with refractory epilepsy who underw ent surgical treatm ent at the First Affiliated H ospital of Fujian M edical U niversity from January 2010 to January 2015.All patients were convenient confirm ed to be FCD by postoperative pathology.The postoperative brain tissue was performed and analyzed,as the experim ental group;of which 30 cases of FCD I,20 cases of FCD域type.At the same time,50 patients with brain injury undergoing decom pression or debridem ent were selected.The norm al brain tissue was removed from the control group.The p-A K T1/2/3(Thr308),H IF-1,VEGF and p-N M D A R2B(Tyr1336)in the brain tissue were detected by im m unohistochem ical staining and W estern blot.The expressions of p-A K T1/2/3(Thr308),H IF-1,VEGF and p-NMDAR2B(Tyr1336)in the epilepsy and norm al brain tissues were observed.The expressions of im m unohistochem istry and茁一actin gray ratio were observed.Results①Various types of refractory epilepsy-related FC D-induced epilepsy in the AKT/H IF/VEGF signaling pathway to varying degrees of activation perform ance were abnorm al phenom ena.②W estern blot:The expression levels of PIF-A K T b 1/2/3(Thr308),H IF-1琢,VEGF and p-N M D A R2B(Tyr1336)in FCD I lesions were(0.619 3±0.078 4),(0.779 2±0.039 1),(0.752 8±0.099 4),(0.641 4±0.091 9)respectively,and th o se in F C D n w ere(0.885 9土0.031 1),(0.862 9±0.035 5),(0.8392±0.0381)and(0.908 8±0.037 3),which were significantly higher than those in the control group of(0.404 2±0.084 9),(0.467 9±0.013 8),(0.479 8±0.045 1)and(0.349 2±0.090 7),the difference was statistically significant(P<0.05).Conclusion The AKT/HIF/VEGF signaling pathway may be involved in the developm ent of F C D-associated refractory epilepsy by regulating NMDA receptor activity.
作者 张扬 方富 林元相 ZHANG Yang;FANG Fu;LIN Yuan-xiang(N eurosurgical D epartm ent,Fujian Provincial H ospital,Fuzhou,Fujian Province,350001 China;2.N eurosurgical D epartm ent,the First H ospital Affiliated to the Fujian M edical U niversity,Fuzhou,Fujian Province,350005 China;N eurosurgical D epartm ent,the First H ospital Affiliated to the Fujian M edical U niversity,Fuzhou,Fujian Province,350005 China)
出处 《中外医疗》 2017年第30期15-17,24,共4页 China & Foreign Medical Treatment
关键词 局灶性皮质发育不良 难治性癫痫 机制 AKT/HIF/VEGF信号通路 NMDA受体 Focal cortical dysplasia Refractory epilepsy M echanism AKT/HIF/VEGF signaling pathway NMDA receptor
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