CAJ | 학술논문

目的：探索缺血再灌注损伤（ I／R）后脑损伤与细胞外组蛋白之间的关系。方法采用改良Longa线栓法建立SD大鼠脑缺血再灌注模型，并在缺血再灌注后1 h、3 h、6 h、12 h、24 h测定循环和大脑局部组蛋白水平。同时培养新生C57－B6小鼠原代皮层神经元并用组蛋白处理细胞，再利用流式细胞技术检测神经细胞的存活率。结果在脑缺血再灌注损伤后，脑局部的细胞外组蛋白浓度在I／R损伤后3 h出现明显升高（ P＜0．05），同时循环组蛋白在12 h后出现显著升高（ P＜0．01），循环组蛋白的升高滞后于局部组蛋白的升高。而细胞外组蛋白可以直接引起原代神经元死亡，在300μg／ml的浓度下神经元的存活率明显下降（ P＜0．05）。结论脑I／R可以引起组蛋白的释放，而细胞外组蛋白可以单独导致神经元死亡。
목적：탐색결혈재관주손상（ I／R）후뇌손상여세포외조단백지간적관계。방법채용개량Longa선전법건립SD대서뇌결혈재관주모형，병재결혈재관주후1 h、3 h、6 h、12 h、24 h측정순배화대뇌국부조단백수평。동시배양신생C57－B6소서원대피층신경원병용조단백처리세포，재이용류식세포기술검측신경세포적존활솔。결과재뇌결혈재관주손상후，뇌국부적세포외조단백농도재I／R손상후3 h출현명현승고（ P＜0．05），동시순배조단백재12 h후출현현저승고（ P＜0．01），순배조단백적승고체후우국부조단백적승고。이세포외조단백가이직접인기원대신경원사망，재300μg／ml적농도하신경원적존활솔명현하강（ P＜0．05）。결론뇌I／R가이인기조단백적석방，이세포외조단백가이단독도치신경원사망。
Objective The objective of this study is to explore the association between extracellular histones and cerebral is?chemic/ reperfusion injury. Methods We managed to build ratcerebral I/R models, anddetected the level of both local and circulating histones. We also culturednew born C57-B6 mice primary cortical neurons. We treated the neurons with histones, then measured the survival rate of neurons by flow cytometer. Results The histones increased 3 hours after I/R injury ( P<0.05) . The elevation of cir?culating histones was not detected until 12 hours after reperfusion, which showed elevation of circulating histonesfollowing elevation of the local ones. We treated culture neurons with 300 μg/ml of calf thymus histones, which significantly decreased survival rate of the cultured neurons. Conclusions Histones can be released into extracellular space following cerebral I/R injury and extracellular his?tones could cause neuron death in vitro .