Romanian Journal of Neurology (Dec 2019)

Ischemic stroke subtypes: Some aspects of apoptosis in acute phase of brain infarction

  • Nataliia Sokhor,
  • Svitlana Shkrobot,
  • Milevska-Vovchuk Lyubov,
  • Olena Venger,
  • Oksana Yasniy

DOI
https://doi.org/10.37897/RJN.2019.4.6
Journal volume & issue
Vol. 18, no. 4
pp. 191 – 199

Abstract

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Objectives. The aim of the given research is to analyze the peculiarities of apoptosis and intracellular oxidative protection in acute phase of different ischemic stroke subtypes. Material and methods. The study included 366 patients. We determined the number of white blood cells in the stage of apoptosis and necrosis, with a high content of reactive oxygen spices, with reduced mitochondrial potential, the activity of Cu, Zn-SOD (superoxide dismutase), Mn-SOD and cathepsin D. Outcomes. We noticed mitochondrial dysfunction, intracellular oxidative stress, apoptosis and necrosis of white blood cells at all subtypes of brain infarction on the 1st day. A direct impact of mitochondrial dysfunction on the course of large arteries atherosclerosis (LAAS) in acute phase was established. In acute phase of LAAS we detect activation of both ways of apoptosis: lysosomal one and apoptosis associated with mitochondrial dysfunction. At LACunar stroke (LAC) we observed activation of mainly lysosomal way of apoptosis, due to the apoptosis of endothelial cells, proved by significant correlation between the content of white blood cells in peripheral blood in the stage of apoptosis (ANV+-cells) and total and free activity of cathepsin D. All ischemic stroke subtypes are associated with significantly (p<0,01) decreased activity of intracellular SOD-dependent antioxidant protective system (total SOD, Mn-SOD and Cu, Zn-SOD), that along with the increased number of intracellular reactive oxygen species (ROS) indicates misbalance between ROS formation process and the possibility of its elimination. At cardioembolic infarct (CEI) neutralization of intracellular ROS is due to mitochondrial SOD activity, while at LAC and LAAS – due to the intracellular one. Conclusions. The peculiarities of apoptosis activity and intracellular antioxidant protection in acute phase of brain infarction depend on its subtype.

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