@article{Barinov E.F._Yevtushenko_Maksimenko_Barinova_Tverdokhleb_Yevtushenko_2013, title={Mechanisms of Inflammation Regulation in the Ischemic Brain (Scientific Review)}, url={https://inj.zaslavsky.com.ua/index.php/journal/article/view/117}, DOI={10.22141/2224-0713.8.62.2013.86078}, abstractNote={<p>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.</p>}, number={8.62}, journal={INTERNATIONAL NEUROLOGICAL JOURNAL}, author={Barinov E.F., Barinov E.F. and Yevtushenko, S.K. and Maksimenko, T.L. and Barinova, M.E. and Tverdokhleb, T.A. and Yevtushenko, I.S.}, year={2013}, month={Nov.}, pages={13–21} }