Effect of Ischemic Postconditioining on Change of Immunoreactivity Level to PECAM-1/CD31 in Rat Neocortex Structures after Global Brain Ischemia

Author:

Shcherbak N. S.1,Gurbo A. G.2,Yukina G. Yu.3,Thomson V. V.3,Shlyakhto E. V.1

Affiliation:

1. Pavlov University; Almazov National Medical Research Centre

2. Almazov National Medical Research Centre

3. Pavlov University

Abstract

Introduction. Ischemic postconditioning (IPostC) of the brain can be considered as a promising approach to limit reperfusion injury in the ischemic area of the brain. Objective – to study the effect of IPostC after global cerebral ischemia on the level of immunoreactivity to PECAM-1/CD31 in the structures of layers II, III and V of the neocortex of rats at different periods of the reperfusion period.Material and methods. In male Wistar rats, a 10-minute global cerebral ischemia was modeled followed by IPostC in the form of reperfusion-ischemia at 15sec/15sec. In the early (2 days) and late (7 days) reperfusion periods after damaging ischemia, the number of morphologically unchanged neurons and the level of immunoreactivity to PECAM-1/CD31 in the structures of layers II, III and V of the neocortex were estimated.Results. It is shown that the use of IPostC by 2 days of reperfusion contributed to the increase in the number of unchanged neurons in layers II and III of 25.8 and 28.2 % (P<0.05), which was not accompanied by changes in the level of immunoreactivity to PECAM-1/CD31, to 7 days of reperfusion there was an increase in the number of unchanged neurons in layers II, III and V of 19.2, 22,1, 21,4 % (P<0.05) was observed a decrease in the level of immunoreactivity to PECAM-1/CD31 in the structures of these layers of 27.4, 39.4, and 16.7 % (P<0.05), respectively, when compared with similar indicators in groups without the use of IPostC.Conlusions. In the mechanisms of physiological reaction formed in the application of ischemic postconditioning after cerebral ischemia and leading to the preservation of the number of unchanged neurons in the late reperfusion period involved PECAM-1/CD31, which suggests that the protective potential of the phenomenon is realized by possible inhibiting the migration of neutrophils, monocytes and lymphocytes and extravasation of leukocytes from the systemic blood flow into the damaged area of the brain, i.e. through suppression of inflammatory response.

Publisher

FSBEI HE I.P. Pavlov SPbSMU MOH Russia

Subject

General Medicine

Reference20 articles.

1. Щербак Н. С., Русакова А. Г., Галагудза М. М. и др. Морфофункциональная характеристика микроциркуляторного русла и нейронов неокортекса после ишемического посткондиционирования // Морфология. – 2016. – Т. 49, № 5. – С. 21–27. [Shcherbak NS, Rusakova AG, Galagudza MM, Yukina GYu, Barantsevich ER, Tomson VV, Shlyakhto EV. Morphofunctional Characteristics of the Microcirculatory Bed and Neurons in the Neocortex after Ischemic Postconditioning. Morfologiia. 2016;49(5):21–27. (In Russ.)]. Doi: 10.1007/s11055-016-0318-6.

2. Щербак Н. С., Овчинников Д. А., Галагудза М. М. и др. Влияние ишемического посткондиционирования на экспрессию белка Bcl-2 в нейронах неокортекса при глобальной ишемии-реперфузии головного мозга у крыс // Трансляц. медицина. – 2016. – Т. 3, № 1. – С. 63–72. [Shcherbak NS, Ovchinnikov DA, Galagudza MM, Yukina GYu, Barantsevich ER, Thomson VV, Shlyakhto EV. Influence Ischemic Postconditioning on Bcl-2 protein expression of neocortex neurons in global cerebral ischemia-reperfusion. Translyacionnaya medicina. 2016;3(1):63–72. (In Russ.)].

3. Hossmann KA. Viability thresholds and the penumbra of focal ischemia. Ann Neurol. 1994;36(4):557–565. Doi: 10.1002/ana.410360404.

4. Васина Л. В., Петрищев Н. Н., Власов Т. Д. Эндотелиальная дисфункция и ее основные маркеры // Регионар. кровообращение и микроциркуляция. – 2017. – Т. 16, № 1 (61). – С. 4–15. [Vasina LV, Petrishchev NN, Vlasov TD. Markers of endothelial dysfunction. Regionarnoe krovoobraŝenie i mikrocirkulâciâ. 2017;16(1(61):4–15. (In Russ.)].

5. Ge H, Wen Y, Yang G, Betz AL. Increased expression of intercellular adhesion molecule-1 in mouse focal cerebral ischemia model. Chin Med J. 2000;113(1):75–79.

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3