Abstract: Stroke is one of leading causes of human disability and death. More than 17 million stroke incidences occur in the world each year. In ischemic stroke (70–80% of all strokes) cerebral vessel occlusion quickly, for few minutes causes oxygen and glucose depletion, ATP deficit, and tissue infarction. It is impossible to rescue neurons in the infarction core. However, the injury propagates to neighboring tissues and forms the transition zone (ischemic penumbra) where cells are damaged slower, for several hours. Protection of penumbra cells and restriction of infarction volume are the main goals of neurologists (Nakka et al., 2008; Chen et al., 2011; Puyal et al., 2013). Despite testing of numerous pro-survival drugs such as glutamate antagonists, blockers of Ca2+ channels, antioxidants, and apoptosis inhibitors, an effective anti-stroke neuroprotector that can rescue neurons within first post-stroke hours is not found yet. Even drugs that protect the ischemic animal brain or cultured neurons in the experiments were either ineffective or caused unacceptable adverse effects in humans (Nakka et al., 2008; Puyal et al., 2013). Therefore, further studies of neurodegeneration and neuroprotection mechanisms in the ischemic penumbra are needed. Unlike ischemic core, where cells die mostly through necrosis, apoptosis prevails in the penumbra (Ferrer, 2006; Radak et al., 2017; Uzdensky, 2019). The dichotomy between necrosis in the infarction core and apoptosis in the penumbra is not strict. Sometimes the signs of apoptotic cell death are revealed in the infarction core.