急性颅脑损伤患者血清中HMGB1及Fas的表达及临床意义

发布时间：2018-03-12 06:46

  本文选题：高迁移率组蛋白B1　切入点：Fas　出处：《济南大学》2013年硕士论文　论文类型：学位论文

【摘要】：目的继发性脑损伤是急性颅脑损伤预后不良的重要因素，脑损伤所引起的脑部和全身的炎症反应的研究和治疗成了临床脑外伤治疗的又一个重要关键点。高迁移率组蛋白B1(High-mobility group box1，HMGB1)在炎症反应中起重要作用，是感染的晚期阶段被释放的炎症因子，但目前研究发现其在脑外伤早期就被大量释放，这一机制目前尚未明确。研究证实， FasL在脑损伤过程中扮演极其重要作用，抑制FasL的作用可以明显减轻脑损伤。Fas(CD95)是传统凋亡受体，以往学者都试图用Fas所导致的致凋亡作用来解释FasL在脑损伤中的作用，有学者在多伦多大学炎症与创伤研究中心发现，FasL（CD178）可以刺激巨噬细胞主动释放HMGB1，这种释放是一个迅速发生的过程。我们提出这样一种假设：在颅脑损伤早期，Fas可通过HMGB1大量释放（非凋亡机制）引起炎症发应导致继发性颅脑损伤。本研究旨在探讨急性颅脑损伤患者血清中HMGB1与Fas的表达及内部联系，进一步明确继发性颅脑损伤发生发展的机制，为颅脑损伤的治疗提供新思路。 方法选择2011年7月至2013年01月在我院就诊的急性颅脑损伤患者62例，，根据患者入院时格拉斯哥昏迷评分(Glasgow coma score GCS)将其分为轻度组（GCS评分＞12分）、中度组（8分＜GCS评分≤12分）和重度组（GCS评分≤8分），选择正常健康志愿者15例做为对照组。所有患者入院后即采集外周静脉血，分离血清，采用双抗体夹心酶联免疫分析法(Enzyme Linked-Immuno-SorbentAssay，ELISA)测定血中HMGB1及Fas含量。采用统计学软件SPSS17.0对所得数据进行处理，并对两组数据进行相关性分析，P0.05为差异有统计学意义。 结果 1、急性颅脑损伤患者血清中HMGB1水平：轻度组为5.23±0.065ng/ml，中度组为8.47±0.075ng/ml，重度组为10.56±0.82ng/ml，对照组为3.54±0.13ng/ml。各组之间差异有统计学意义（P＜0.05）。 2、急性颅脑损伤患者血清中Fas水平：轻度组为2.83±0.13pg/ml，中度组为4.55±0.13μpg/ml重度组为7.31±0.19pg/ml，对照组为1.10±0.63pg/ml，各组之间差异有统计学意义（P＜0.05）。 3、相关分析发现急性颅脑损伤患者血清中Fas和HMGB1水平呈正线性相关关系，r=0.875，P＜0.05。 结论 1、急性颅脑损伤患者血清中HMGB1和Fas可判断患者病情轻重。 2、急性颅脑损伤患者血清中Fas的升高可能是通过HMGB1-炎症反应途径导致继发性颅脑损伤。
[Abstract]:Objective Secondary brain injury is an important factor in poor prognosis of acute brain injury. The study and treatment of brain and systemic inflammation induced by brain injury has become another key point in the treatment of brain trauma. High mobility group box 1 HMGB1 plays an important role in the inflammatory response. It is an inflammatory factor released in the late stage of infection, but it has been found to be released in large quantities in the early stage of brain injury. This mechanism is not clear at present. It has been confirmed that FasL plays an extremely important role in the process of brain injury. Inhibition of FasL can significantly reduce brain injury. Fas-CD95) is a traditional apoptotic receptor. Previous scholars have tried to explain the role of FasL in brain injury by using the apoptosis-induced effect of Fas. Some researchers at the Center for inflammation and Trauma of the University of Toronto have found that FasL CD178) stimulates the active release of HMGB1 from macrophages, which is a rapid process. We propose a hypothesis that FAS can be activated in the early stages of craniocerebral injury. Excessive release of HMGB1 (non-apoptotic mechanism) may induce inflammation and lead to secondary craniocerebral injury. The purpose of this study was to investigate the expression of HMGB1 and Fas in serum of patients with acute craniocerebral injury. To further clarify the mechanism of the occurrence and development of secondary craniocerebral injury and provide a new way for the treatment of craniocerebral injury. Methods 62 patients with acute craniocerebral injury were selected from July 2011 to January 2013. According to the Glasgow coma score score on admission, the patients were divided into mild group (GCS > 12), moderate group (8 < GCS 鈮

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