E.V. Uzlova *S.M. Zimatkin **E.I. Bon ***

Grodno State Medical University, Grodno, 230009 Republic of Belarus

E-mail: *uzlovaliza@gmail.com**smzimatkin@mail.ru***asphodela@list.ru

Received June, 2022; Accepted July 18, 2022

 

ORIGINAL ARTICLE

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DOI: 10.26907/2542-064X.2023.2.204-215

For citation: Uzlova E.V., Zimatkin S.M., Bon E.I. Neuroglobin content in rat brain structures after subtotal cerebral ischemia. Uchenye Zapiski Kazanskogo Universiteta. Seriya Estestvennye Nauki, 2023, vol. 165, no. 2, pp. 204–215. doi: 10.26907/2542-064X.2023.2.204-215. (In Russian)

Abstract

Neuroglobin (Ngb) is a member of the globin family. Like other globin proteins, it is involved in the maintenance of oxygen homeostasis. Ngb distribution in the normal brain is well known, but its response to pathological injury, such as cerebral ischemia, has not yet been adequately elucidated. One primary reason for this is that ischemic lesions in cerebral tissues have mostly been studied in transgenic organisms. In addition, the available data on Ngb content are limited to a small number of brain structures. This article examines the patterns of changes in Ngb immunoreactivity in neurons from different parts of the rat brain after subtotal cerebral ischemia of varying duration. An immunohistochemical study of Ngb content in 25 brain structures of white male Wistar rats exposed to 30-min and 3-h subtotal cerebral ischemia was performed. A decrease in Ngb content in all structures (especially 3 h after the ischemia onset and in the phylogenetically older parts), temporal mediation, and dependence on the phylogenetic age were revealed. The obtained results further decipher the correlation between the changes in Ngb content and the degree of cerebral ischemic damage, which is necessary to clarify the functions of the studied protein.

Keywords: neuroglobin, ischemia, neurons, brain, rat

Acknowledgements. This study was funded by the Belarusian Republican Foundation for Fundamental Research (agreement no. М21М-054 of July 1, 2021 “Evaluation of the energy potential and oxygen depot of brain neurons to predict their sensitivity to ischemia”).

Figure Captions

Fig. 1. Immunohistochemical staining of neurons in the telencephalon: a–c – piriform cortex, layer II, d–f – hippocampus, field CA2, pyramidal layer; a and d – control group, b and e – 30-min subtotal cerebral ischemia, c and f – 3-h subtotal cerebral ischemia. Magnification 400x.

Fig. 2. Immunohistochemical staining of neurons in the diencephalon and medulla oblongata: a – c – medial habenular nucleus, d–f – gigantocellular nucleus; a and d – control group, b and e – 30-min subtotal cerebral ischemia, c and f – 3-h subtotal cerebral ischemia. Magnification 400x.

Fig. 3. Immunohistochemical staining of neurons in the cerebellum: a–c – Purkinje cells of the cerebellar cortex, d–f – neurons of the lateral nucleus: a and d – control group, b and e – 30-min subtotal cerebral ischemia, c and f – 3-h subtotal cerebral ischemia. Magnification 400x.

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