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沙鼠脑缺血及缺血耐受模型中海马热休克蛋白-27的免疫组织化学研究

An immunohistochemical study of heat shock protein-27 in the hippocampus in a gerbil model of cerebral ischemia and ischemic tolerance.

作者信息

Kato H, Araki T, Itoyama Y, Kogure K, Kato K

机构信息

Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Neuroscience. 1995 Sep;68(1):65-71. doi: 10.1016/0306-4522(95)00141-5.

DOI:10.1016/0306-4522(95)00141-5
PMID:7477936
Abstract

Preconditioning of the gerbil brain with a 2-min period of sublethal ischemia protects against neuronal damage following a subsequent 3-min period of ischemia which normally damages CA1 neurons of the hippocampus (ischemic tolerance). In this study, we investigated the role of a small stress protein, heat shock protein-27, in the induction of ischemic tolerance. For this purpose, we used immunohistochemistry with an antibody against heat shock protein-27. Normal hippocampus contained very low levels of heat shock protein-27. The preconditioning ischemia for 2 min caused little changes in the heat shock protein-27 immunostaining in CA1 neurons but an increase in heat shock protein-27 immunostaining in a small number of astrocytes in the CA3 region and in many astrocytes in the dentate hilus. The second ischemia for 3 min caused no specific changes in heat shock protein-27 immunostaining in CA1 neurons both with and without tolerance in early reperfusion periods. After seven days, destruction of CA1 neurons occurred in animals without preconditioning and reactive astrocytes were intensely immunostained for heat shock protein-27. An intense heat shock protein-27 immunostaining was also seen in astrocytes in the dentate hilus after the second ischemia in both groups. Thus, we observed no temporal correlation between the induction of heat shock protein-27 and the manifestation of ischemic tolerance in the CA1 neurons. Most intense heat shock protein-27 immunostaining was observed in reactive astrocytes that accumulated in the damaged CA1 region and dentate hilus.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

用2分钟亚致死性缺血对沙鼠脑进行预处理,可保护其免受随后3分钟缺血所致的神经元损伤(缺血耐受),而该时长的缺血通常会损伤海马体的CA1神经元。在本研究中,我们调查了一种小应激蛋白——热休克蛋白27在诱导缺血耐受中的作用。为此,我们使用了针对热休克蛋白27的抗体进行免疫组织化学研究。正常海马体中热休克蛋白27的含量极低。2分钟的预处理缺血对CA1神经元中热休克蛋白27免疫染色几乎没有影响,但CA3区少量星形胶质细胞和齿状回门区许多星形胶质细胞中的热休克蛋白27免疫染色增加。在早期再灌注期,无论有无耐受性,3分钟的第二次缺血对CA1神经元中热休克蛋白27免疫染色均无特异性影响。七天后,未进行预处理的动物中CA1神经元发生破坏,反应性星形胶质细胞热休克蛋白27免疫染色强烈。两组第二次缺血后,齿状回门区星形胶质细胞中也可见强烈的热休克蛋白27免疫染色。因此,我们未观察到热休克蛋白27的诱导与CA1神经元缺血耐受表现之间的时间相关性。在受损的CA1区和齿状回门区积聚的反应性星形胶质细胞中观察到最强的热休克蛋白27免疫染色。(摘要截选至250字)

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