Wistar大鼠缺血性脑卒中后脑组织蛋白酶体活性变化。

O. Savchuk, M. Orlovsky, Ie. S. Iarmoliuk, S. Goncharov, V. Dosenko, G. Skibo
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引用次数: 1

摘要

局灶性缺血性病变后,脑组织的功能和结构重组发生在周围和远端脑区。特别是,反应性或再生过程已被描述为发生在梗死区域和对侧半球。实验选用大鼠63只,分为3组(每组21只):假手术组、短期大脑中动脉闭塞组和长期大脑中动脉闭塞组。我们用小泉J法研究了大脑中动脉短暂闭塞时蛋白酶体蛋白水解的变化,持续时间2和60 min,比较了不同类型蛋白酶体活性的变化和缺血性损伤的严重程度,发现脑组织蛋白水解活性降低了三种类型(胰蛋白酶-型,糜凝胰蛋白酶样,肽酰谷氨酰肽水解)。短期MCAO组脑缺血区凝乳胰蛋白酶样活性较对照组降低4.1倍(P > 0.05),长期MCAO组脑缺血区凝乳胰蛋白酶样活性较对照组降低5.8倍(P < 0.05)。短期MCAO大鼠脑缺血区胰蛋白酶样活性较对照组降低7.1倍(P > 0.05),长期MCAO大鼠脑缺血区胰蛋白酶样活性较对照组降低12.5倍(P < 0.05)。短期MCAO组缺血区PGPH活性较对照组降低8倍(P > 0.05),长期MCAO组缺血区PGPH活性较对照组降低2.8倍(P < 0.05)。在再灌注6 h时,大脑半暗区和核心区也有类似的动态变化,长期来看,核心区和对侧区之间没有显著差异。我们的研究结果表明,蛋白酶体活性也可能在局灶性脑缺血后对侧皮质可塑性中发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Proteasomal activity in brain tissue following ischemic stroke in Wistar rats.
Functional as well as structural reorganization of brain tissues takes place in the surrounding and remotes brain areas after focal ischemic lesions. In particular, reactive or regenerative processes have been described to occur in the infarction areas and the contralateral hemisphere. Experiments were performed on 63 rats, divided into 3 groups (each consisted of 21 animals): sham operated, short-term occlusion of the right middle cerebral artery (MCAO) group, and long-term MCAO group. We have studied changes in proteasome proteolysis during transient occlusion of the middle cerebral artery using method of Koizumi J., duration 2 and 60 min and made the comparison between changes in different types of proteasome activity and severity of ischemic injury and showed three types of decrease inproteolytic activity (trypsin-, chymotrypsin-like, peptidylglutamyl peptide-hydrolyzing) in the brain tissues. Chymotrypsin-like activity of ischemic areas of the brain for short-term MCAO decreased 4.1 times compared with controls (P > 0.05), for long-term MCAO decreased 5.8 times compared with controls (P < 0.05). Trypsin-like activity of ischemic areas of brain for short-term MCAO decreased 7.1 times compared with controls (P > 0.05), for long-term MCAO decreased 12.5 times compared with controls (P < 0.05). PGPH activity of ischemic areas for short-term MCAO decreased 8 times compared with controls (P > 0.05), for long-term MCAO decreased 2.8 times compared with controls (P < 0.05). The similar dynamics was observed also in the penumbra and the core zone of the brain at 6 h of reperfusion, in the long run there is no significant difference between the core and contralateral zones. Our results suggest that proteasome activity may play also a role in contralateral cortical plasticity occurring after focal cerebral ischemia.
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