The aim of our study was to study leukocyte apoptosis and to establish its relationship with changes of cognitive function in patients with chronic brain ischemia (CBI) and hydrocephalus (HC). A comprehensive examination of 110 patients with CBI and HC was performed. Indicators of apoptosis, mitochondrial dysfunction, intracellular oxidative stress were studied by cytofluorimetric method. Significantly higher indicators of ANV+-, PI+-, APK+- and Mito+-cells in the presence of HC. In the group of men, the inverse correlation between the content of AnV+-cells and the result of the MoCA-test — r = –0.42; p = 0.006, in women — r = –0.51; p = 0.005. A significant relationship was found between the content of APK+- and ANV+- cells (r = 0.67, p = 0.003) and between the number of APK+- and PI+-cells (r = 0.73, p = 0.002) in patients aged 60—74. In patients with dementia progression, a moderate relationship was found between the level of cognitive functioning and the proportion of cells in the early stage (ANV+-cells) (r = –0.50; p = 0.026) and late (PI+-cells) (r = –0.30; p = 0.041) apoptosis. In the group of patients with mild and moderate cognitive deficits, correlations between the MoCA scale result and the content of ANV+-cells were recorded at the level of moderate — (r = –0.37; p = 0.040) and PI+-cells at the level of weak (r = –0.24; p = 0.049). Significantly (p < 0.05) higher content of leukocytes in the stage of apoptosis and necrosis and leukocytes with increased content of intracellular APK and with reduced mitochondrial potential compared to patients without HC was found in patients with CBI with HC. There is a significant difference between the values of indicators in middle-aged and elderly patients and indicators of patients older 74 years. The progression of neurological and cognitive deficits was accompanied by an increase of the production of ANV+-, APK+- and Mito+-cells. The highest proportion of ANV+- and PI+-cells was detected in the presence of a combination of dementia, extrapyramidal syndrome and gait apraxia in patients with CBI with HC.
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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