Pathophysiology of Ischemic Stroke: Role of Oxidative Stress

Abstract

<jats:sec> <jats:title>:</jats:title> <jats:p>Stroke is the second leading cause of mortality and the major cause of adult physical disability worldwide. The current available treatment to recanalize the blood flow in acute ischemic stroke is intravenous administration of tissue plasminogen activator (t-PA) and endovascular treatment. Nevertheless, those treatments have the disadvantage that reperfusion leads to a highly harmful reactive oxygen species (ROS) production, generating oxidative stress (OS), which is responsible for most of the ischemia-reperfusion injury and thus causing brain tissue damage. Also, OS can lead brain cells to apoptosis, autophagy and necrosis. The aims of this review are to provide an updated overview of the role of OS in brain IRI, providing some bases for therapeutic interventions based on counteracting the OS-related mechanism of injury and thus suggesting novel possible strategies in the prevention of IRI after stroke.</jats:p> </jats:sec>

Brain acute ischemia mechanisms: implications to experimental and clinical treatment

“…Подвергнутые ишемии различной степени выраженности нейроны, клетки нейроглии и эндотелиальные клетки сосудов головного мозга переносят воздействие внутриклеточных метаболических нарушений, сдвига ионного баланса и осмотического статуса, летальной деполяризации, кальциевой перегрузки, образования свободных радикалов и других токсичных соединений, иммунной реакции с элементами аутоиммунитета, эксайтотоксичных медиаторов [31][32][33][34][35][36][37].…”

Neuroprotective Function of High Glycolytic Activity in Astrocytes: Common Roles in Stroke and Neurodegenerative Diseases

“…Peroxisome is an organelle where very long chain fatty acids (>C22) are metabolized [ 10 , 11 ]. Although ROSs act as important signal molecules, in general, ROSs are regarded to play detrimental roles in cell injury [ 9 , 12 , 13 , 14 ]. Thus, several intrinsic protective mechanisms operate to reduce the toxic effects of ROSs in the brain.…”

“…Thus, several intrinsic protective mechanisms operate to reduce the toxic effects of ROSs in the brain. The dysfunction of these intrinsic mechanisms by which the brain eliminates ROSs leads to both acute [ 9 , 12 , 13 , 14 ] and chronic [ 15 , 16 ] neuronal damage. In ischemic stroke, for example, the elimination of ROSs during reperfusion therapy by either pharmacological thrombolysis or a mechanical thrombectomy is an essential therapeutic strategy, since damaged mitochondria during ischemia serve as a potential source of massive ROS production, especially after reperfusion.…”

“…Initial ischemia-induced cytotoxic edema, which is a reflection of energy failure, is followed by vasogenic edema that reflects an increased permeability of blood–brain barrier. In addition to ROS elimination, the development of effective treatment of brain edema is imperative [ 12 , 13 , 14 , 19 , 20 , 21 , 22 ]. Likewise, accumulated cellular damage caused by chronic ROS production might also be a potential mechanism of age-related neuronal damage, i.e., neurodegenerative diseases including Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis (ALS).…”

Compatibility of ingredients of Danshen (Radix Salviae Miltiorrhizae) and Honghua (Flos Carthami) and their protective effects on cerebral ischemia‑reperfusion injury in rats

“…In 2008, an epidemiological survey indicated that strokes, with an incidence of 136.64 per 100,000 individuals, had replaced cancer as the leading cause of mortality in China ( 5 ). At present, intravenous thrombolytic therapy is the main clinical treatment for ischemic stroke ( 1 , 6 ), and there is still a lack of effective drugs to protect neurons from death. Therefore, there is a need for multi-target and improved therapeutic drugs, which is why the beneficial effects of Traditional Chinese Medicine (TCM) is worth investigating ( 7 ).…”