人不同程度肝硬化星形胶质细胞关键标志物的免疫组化研究

IF 0.1 Q4 MEDICINE, GENERAL & INTERNAL
T. Shulyatnikova, V. Tumanskyi
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引用次数: 2

摘要

本研究的目的是测定不同程度肝硬化条件下人脑不同区域GFAP、GS和AQP4的免疫组化水平。材料和方法。本研究采用Child-Pugh分级法对90例终生患有非酒精性肝硬化的A级(n = 30,“A”组)、B级(n = 30,“B”组)和C级(n = 30,“C”组)患者的断面资料进行分析,其中59例(65.55%)临床症状为I-IV级肝性脑病。采用免疫组化方法检测大鼠皮质、白质、海马、丘脑、纹状体、小脑的GFAP、GS、AQP4水平。从肝硬化A级到C级,GFAP表达逐渐降低。GFAP下降最多的是C类皮层和丘脑(分别下降6.74倍和6.23倍)。与GFAP相反,随着肝硬化的加重,GS的表达逐渐升高。“C”组GS增强最显著的部位是皮质和丘脑,分别增加4.34倍和4.26倍。AQP4水平也呈现与肝硬化加重相关的生长模式。在“C”组中,大脑皮层和丘脑增加最多(分别增加4.25倍和4.34倍)。从B类开始,GFAP、GS和AQP4水平的变化呈区域依赖关系。GFAP与GS、GFAP与AQP4蛋白在6个研究区域均呈正相关,而GFAP与GS、GFAP与AQP4蛋白呈负相关。早在肝硬化A级时,脑星形胶质细胞中就发生了动态的分子改变,表明星形胶质细胞重构的进行性发展,破坏了其细胞骨架和细胞内分子结构域的重新分配。这种现象具有区域和时间特异性;随着时间的推移,其症状随着课程的增加而增强,在c课中表现得最为明显。在研究的大脑区域中,皮层和丘脑的蛋白质变化最为明显。从B类开始,正反两种类型的分子变化关系显著。同时出现的联系可能表明这些分子在慢性肝性脑病星形胶质细胞重塑中的协同参与。上述星形胶质细胞分子复合物的改变既可以作为肝硬化期间反应性星形胶质细胞增生的诊断标志物,也可以作为肝硬化患者脑病新治疗方法的靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Key astroglial markers in human liver cirrhosis of different degree: immunohistochemical study
The aim of the study – determining the immunohistochemical levels of the GFAP, GS and AQP4 in different regions of the human brain in the conditions of liver cirrhosis of different degree. Materials and methods. The study was performed on sectional material of 90 patients who suffered during lifetime from liver non-alcoholic cirrhosis of classes A (n = 30, group “A”), B (n = 30, group “B”) and C (n = 30, group “C”) according to Child–Pugh classification, including 59 (65.55 %) cases with clinical symptoms of I–IV grade hepatic encephalopathy. Cortex, white matter, hippocampus, thalamus, striopallidum, cerebellum, were examined using immunohistochemical method for evaluation of GFAP, GS and AQP4 levels. Results. GFAP expression gradually decreased from classes A to C of cirrhosis. The most expressed GFAP decline was found in class C in the cortex and thalamus (6.74- and 6.23-fold decrease). Contrary to GFAP, GS expression gradually increased along with aggravation of cirrhosis. The most prominent augmentation of GS was related in the cortex and thalamus in “C” group, respectively 4.34- and 4.26-fold increase. AQP4 levels also showed growing mode correlated with cirrhosis aggravation. The highest increase was found in the cortex and thalamus in “C” group (4.25- and 4.34-fold increase, respectively). Starting from class B, altered GFAP, GS, and AQP4 levels showed region-dependent relationships. GS and AQP4 were positively correlated in all 6 studied regions, while the inverse relationships were found between GFAP vs. GS and GFAP vs. AQP4 proteins. Conclusions. As early as in class A of cirrhosis, dynamic molecular alterations are occurred in the brain astrocytes, indicating the progressive development of astroglial remodeling with a violation of its cytoskeleton and redistribution of molecular domains within cells. This phenomenon is region- and time-specific; its signs get stronger with time from class to class, becoming most pronounced in class C. Among studied brain regions, cortex and thalamus are characterized by the most pronounced protein changes. Starting from class B, the remarkable relationship is seen between molecular changes of both direct and inverse type. Simultaneously emerging links might indicate synergistic involvement of these molecules in astroglial remodeling in chronic hepatic encephalopathy. Alterations in the mentioned astroglial molecular complex can serve both as a diagnostic marker of reactive astrogliosis during liver cirrhosis and represent a target for novel therapeutic approaches regarding encephalopathy in cirrhotic patients.
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来源期刊
Zaporozhye Medical Journal
Zaporozhye Medical Journal MEDICINE, GENERAL & INTERNAL-
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