Expression of NF-L protein in the sensorimotor cortex during the modeling of transient ischemia against the background of sensitization by brain antigen and immunocorrection of the changes

Authors

  • L. M. Yaremenko Bogomolets National Medical University, Kyiv, Ukraine,
  • A. N. Grabovoy Ukrainian National Cancer Institute, Kyiv, Ukraine,
  • L.P. Bidna Bogomolets National Medical University, Kyiv, Ukraine,
  • S. Ye. Shepelev Bogomolets National Medical University, Kyiv, Ukraine,
  • M. M. Grusha Bogomolets National Medical University, Kyiv, Ukraine,

DOI:

https://doi.org/10.14739/2310-1237.2018.1.129443

Keywords:

ischemia, NF-L-protein (NFР-L), central nervous system sensitization, immunomodulation

Abstract

Aim. To study the levels of NFР-L protein expression in the sensorimotor cortex of rats in the simulation of transient ischemia against the background of sensitization by the brain antigen and immunocorrection of the resulting changes by imunofan.

Materials and methods. The study was conducted on 185 male mature white rats from Wistar line weighted 260–290 g, in which the damage of the brain was modulated. The brain for study was taken on the 1st, 3rd, 10th, 30th and 90th days after the start of the experiment. The histological, immunehistochemical, morphometric and statistical methods were used.

Results. Observations have shown that sensitization with the brain antigen causes diffuse degenerative changes in the cerebral cortex and a decrease in NFP-L expression. This background leads to an increase in the severity of brain damage in acute circulatory disturbances compared with when no sensitization was performed.

After transient ischemic attack, the recovery period was significantly less than in the absence of sensitization, rounded corpuscles with a relatively high level of expression of NFР-L, which we qualified as nerve growth flasks (cones). This allows us to say that sensitization by the brain antigen delays the regeneration of nerve fibers, which is an important component of compensatory-recovery processes in the cerebral cortex after ischemic attack.

Imunofan under the conditions of modeling of combined immune-vascular lesions of the brain had protective properties and reduced the severity of the decrease in NFР-L expression. We attribute these effects of imunofan, especially in the recovery period after brain damage in the first place, to its immunomodulatory effect which is confirmed by comparing the dynamics of the restoration of NFР-L expression in the affected and contralateral hemispheres, where the latter experienced immune damage in the absence of ischemia.

Conclusions. Sensitization by the brain antigen leads to diffuse degenerative changes in the cerebral cortex, which are accompanied by a decrease in the expression of NFР-L. Previous sensitization by brain antigen in acute impairment of cerebral circulation leads to increased severity of brain damage and decreased expression of NFР-L, slows and changes the dynamics of its recovery. The effect of immunophan use is to reduce changes in NFР-L expression in the sensorimotor cortex caused by both sensitization with the brain antigen and in combination with transient impairment of cerebral blood flow.

 

References

Zozulia, А. І., Slabkyi, H. O., & Zozulia, І. S. (2014). Problemy, yaki stoiat pered doslidnykamy shodo tserebrovaskuliarnykh khvorob v tsilomu ta insultu zokrema. [Problems facing researchers regarding cerebrovascular diseases in general and stroke in particular]. Ukrainskyi medichyi chasopys, 5, 112–120 [in Ukrainian].

Vickers, J. C., Kirkcaldie, M. T., Phipps, A., & King, A. E. (2016). Alterations in neurofilaments and the transformation of the cytoskeleton in axons may provide insight into the aberrant neuronal changes of Alzheimer’s disease. Brain research bulletin, 126(3), 324–333. doi: 10.1016/j.brainresbull.2016.07.012.

Härtig, W., Krueger, M., Hofmann, S., Preißler, H., Märkel, M., Frydrychowicz, C., et al. (2016). Up-regulation of neurofilament light chains is associated with diminished immunoreactivities for MAP2 and tau after ischemic stroke in rodents and in a human case. J Chem Neuroanat, 78, 140–148. doi: 10.1016/j.jchemneu.2016.09.004.

Miró-Mur, F., Urra, X., Gallizioli, M., Chamorro, A., & Planas, A. M. (2016). Antigen presentation after stroke. Neurotherapeutics, 13(4), 719–728.

Park, M. G., Kim, M. K., Chae, S. H., Kim, H. K., Han, J., & Park, K. P. (2017). Lymphocyte-to-monocyte ratio on day 7 is associated with outcomes in acute ischemic stroke. Neurological Sciences, 39(2), 243–249. doi: 10.1007/s10072-017-3163-7.

Liesz, A., Zhou, W., Mracsko, E., Karcher S., Bauer H., Schwarting S., et al. (2011) Inhibition of lymphocyte trafficking shields the brain against deleterious neuroinflammation after stroke. Brain, 134(3), 704–720. doi: 10.1093/brain/awr008.

Lebedev, V. V., & Novikov, S. A. (2006) Gidrofil'nyj geksapeptid imynofan –giperaktivnyj regulyator transportnykh belkov mnozhestvennoj lekarstvennoj ustojchivosti [Hydrophilic hexapeptide imunofan - hyperactive regulator of transport proteins of multiple drug resistance]. Byulleten' e'ksperimental'noj biologii i mediciny, 142(12), 649–651 [in Russian].

Hrabovyi, O. M., & Yaremenko, L. M. (patentee) (2008). Patent 36843, MPK G09B 23/00, Ukraina. Sposib modeliuvannia kombinovanoho sudynno-imunnoho poshkodzhennia mozku [Patent 36843, IPC G09B 23/00, Ukraine. Method of modeling of combined vascular-immune brain damage]. Biuleten, 21. [in Ukrainian].

Yaremenko, L. M., & Grabovoy, A. N. (2016) Changes in the expression of neurofilament protein in the rat sensorimotor cortex induced by microembolization of blood vessels: effect of immunomodulation. Neurophysiology, 48(2), 111–116.

Ueno, Y., Chopp, M., Zhang, L., Buller, B., Liu, Z., Lehman, N. L., et al. (2012). Axonal outgrowth and dendritic plasticity in the cortical peri-infarct area after experimental stroke. Stroke, 43(8), 2221–2228. doi: 10.1161/STROKEAHA.111.646224.

Downloads

How to Cite

1.
Yaremenko LM, Grabovoy AN, Bidna L, Shepelev SY, Grusha MM. Expression of NF-L protein in the sensorimotor cortex during the modeling of transient ischemia against the background of sensitization by brain antigen and immunocorrection of the changes. Pathologia [Internet]. 2018May3 [cited 2024Nov.2];(1). Available from: http://pat.zsmu.edu.ua/article/view/129443

Issue

No. 1 (2018)

Section

Original research

License

Authors who publish with this journal agree to the following terms:

    1. Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
Лицензия Creative Commons
    1. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.

  1. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (SeeThe Effect of Open Access).