CXCL13和CXCR5在难治性颞叶癫痫患者和癫痫大鼠脑组织中的表达变化

发布时间：2018-07-12 19:02

本文选题：CXCL13 + CXCR5　；参考：《重庆医科大学》2017年硕士论文

【摘要】：目的:癫痫的发病机制目前仍然不清楚。最近的研究表明,大脑的炎症过程在癫痫形成中很常见且起到至关重要的作用。而C-X-C趋化因子配体13(CXCL13)及其唯一受体C-X-C趋化因子受体5(CXCR5)在中枢神经系统(CNS)中高度表达并参与炎症反应。本研究旨在评估CXCL13和CXCR5在难治性癫痫(IE)患者和颞叶癫痫(TLE)模型(氯化锂-匹鲁卡品点燃)大鼠的脑组织中的表达,以确定CXCL13-CXCR5信号通路在癫痫形成中的作用。方法:1.收集20例难治性颞叶癫痫患者的颞叶皮质标本和20例脑外伤患者的组织学正常颞叶皮质标本。2.SD大鼠腹腔注射氯化锂-匹鲁卡品建立慢性癫痫模型,对照组大鼠腹腔注射生理盐水。3.使用免疫荧光双标技术研究颞叶癫痫患者和癫痫大鼠脑组织中CXCL13和CXCR5的细胞定位。实时荧光定量聚合酶链反应(RT-q PCR)、免疫组织化学、蛋白印迹方法测定各组CXCL13和CXCR5的mRNA和蛋白表达量的变化。结果:免疫荧光双标结果显示CXCL13主要表达在神经元和星形胶质细胞的细胞膜和细胞质中,而CXCR5主要表达在神经元的细胞膜和细胞质中。研究发现CXCL13和CXCR5的mRNA表达水平与蛋白表达水平在TLE患者和TLE大鼠中显着升高。此外,在匹鲁卡品癫痫模型大鼠中,CXCL13和CXCR5的蛋白表达水平在首次发作达到癫痫持续状态(SE)之后的不同时间阶段有不同的改变趋势,这些癫痫阶段包括急性期(6、24和72小时组),潜伏期(7和14天组)和慢性期(30和60天组)。结论:CXCL13和CXCR5在难治性颞叶癫痫患者和癫痫大鼠的脑组织中表达升高。CXCL13-CXCR5信号通路可能在IE中发挥了致病作用。CXCL13和CXCR5可能作为一种在癫痫患者大脑中表达的潜在的炎症相关生物标志物。
[Abstract]:Objective: the pathogenesis of epilepsy is still unclear. Recent studies have shown that inflammation in the brain is common and critical in epilepsy formation. C-X-C chemokine ligand 13 (CXCL13) and its only receptor, C-X-C chemokine receptor 5 (CXCR5), are highly expressed in the central nervous system (CNS) and participate in inflammatory reactions. The purpose of this study was to evaluate the expression of CXCL13 and CXCR5 in the brain of patients with intractable epilepsy (IE) and rats with temporal lobe epilepsy (TLE), and to determine the role of CXCL13-CXCR5 signaling pathway in epileptogenesis. Method 1: 1. The temporal cortex specimens of 20 patients with refractory temporal lobe epilepsy and the normal temporal cortex specimens of 20 patients with brain trauma were collected. 2. SD rats were injected intraperitoneally with lithium chloride-pilocarpine to establish a chronic epilepsy model. Rats in control group were intraperitoneally injected with normal saline. The cellular localization of CXCL13 and CXCR5 in the brain of temporal lobe epilepsy patients and epileptic rats was studied by immunofluorescence double labeling technique. The mRNA and protein expressions of CXCL13 and CXCR5 were detected by real-time fluorescence quantitative polymerase chain reaction (RT-q PCR), immunohistochemistry and Western blot. Results: immunofluorescence double labeling results showed that CXCL13 was mainly expressed in the cell membrane and cytoplasm of neurons and astrocytes, while CXCR5 was mainly expressed in the cell membrane and cytoplasm of neurons. It was found that the mRNA and protein expression levels of CXCL13 and CXCR5 were significantly increased in TLE patients and TLE rats. In addition, the protein expression levels of CXCL13 and CXCR5 in Pilucapine epileptic model rats showed different trends at different time stages after the onset of epileptic status (SE). These epileptic stages included acute (6o 24 and 72 h), latency (7 and 14 days) and chronic (30 and 60 days). Conclusion the increased expression of CXCL13 and CXCR5 in the brain of intractable temporal lobe epilepsy patients and epileptic rats. CXCL13-CXCR5 signaling pathway may play a pathogenic role in IE. CXCL13 and CXCR5 may be a potential inflammation expressed in the brain of epileptic patients. Disease related biomarkers.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R742.1

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