Mechanisms of Inflammation Regulation in the Ischemic Brain (Scientific Review)

Authors

  • Barinov E.F. Barinov E.F. Donetsk National Medical University named after M. Gorky, Donetsk, Ukraine
  • S.K. Yevtushenko Donetsk National Medical University named after M. Gorky, Donetsk, Ukraine
  • T.L. Maksimenko Donetsk National Medical University named after M. Gorky, Donetsk, Ukraine
  • M.E. Barinova Donetsk National Medical University named after M. Gorky, Donetsk, Ukraine
  • T.A. Tverdokhleb Donetsk National Medical University named after M. Gorky, Donetsk, Ukraine
  • I.S. Yevtushenko Donetsk National Medical University named after M. Gorky, Donetsk, Ukraine

DOI:

https://doi.org/10.22141/2224-0713.8.62.2013.86078

Keywords:

stroke, ischemic brain, leukocytes, microglia, the mechanisms of inflammation

Abstract

This scientific review substantiates the role of leukocytes and microglia in the pathogenesis of inflammation in ischemic brain. Primary neuronal damage occurs within a few minutes after ischemia, while the inflammatory response, contributing to the progression of disease can last from a few days to several months. The attention in focused on the fact that the migration of neutrophils into the brain parenchyma and secretion of proteases — one of the main causes of neurons’ and glia death in reperfusion and delayed brain injury. There is discussed the role of integrin, CXCR1/2 chemokine receptors, TNF-α, TLR2 and TLR4, Slit1-protein, angiotensin II, epinephrine and serotonin in the modulation of the functional activity of leukocytes. It has been shown that increased blood-brain barrier permeability is mediated by P2Y2 receptors related to G-protein, causing an increase in intracellular Ca2+, and by P2Y1 receptors affecting by inhibition of adenylate cyclase. Interest in lymphocytes is dictated by the presence of lymphopenia after a stroke that creates the possibility of autoimmune inflammation in this cohort of patients. These authors’ data confirm the fact that after cerebral ischemia monocytes/macrophages are activated through chemokine receptor CCR2 and act indirectly through TGF-β1, required to maintain the functional integrity of the neurovascular complex.

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Published

2013-11-01

How to Cite

Barinov E.F., B. E., Yevtushenko, S., Maksimenko, T., Barinova, M., Tverdokhleb, T., & Yevtushenko, I. (2013). Mechanisms of Inflammation Regulation in the Ischemic Brain (Scientific Review). INTERNATIONAL NEUROLOGICAL JOURNAL, (8.62), 13–21. https://doi.org/10.22141/2224-0713.8.62.2013.86078

Issue

Section

Scientific Review

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