The Effects of NEES on PARP Expression and Cell Death in Rat Cerebral Cortex After Ischemic Injury

Strokes are one of the top three leading causes of death in South Korea. Treatment requires a great amount of time, effort and money. Along with a rise in adult diseases due to increased longevity and changes in eating and living habits, the number of stroke incidents that occur each year is also growing(1). Themost common cause of stroke is ischemia, caused by ischemic conditions or trauma, and it is known to be related to synaptic plasticity and apoptosis(2). Neuron apoptosis can occur without severe trauma or direct brain tissue damage. It can occur in longterm and repetitive conditions(3, 4), and necrosis occurs not only in the directly affected area but also in surrounding areas due to secondary effects such as increased intracranial pressure, hypoxia, and ischemia(5). These surrounding areas, which cause cell death, show decreased brain perfusion due to hypoxic and ischemic condition. However, there is a penumbra area in which ATP metabolism and ion homeostasis through cell membrane are maintained(6). Through appropriate treatment after hypoxic and ischemic brain damage, it is possible to recover function in such areas. It is also known that cell death in penumbra areas are mainly caused by cell apoptosis(7). Hypoxic and ischemic brain damage causes external inflammatory reactions, including depositionandaccumulationofmacrophages,aswellas The Effects of NEES on PARP Expression and Cell Death in Rat Cerebral Cortex After Ischemic Injury