Abstract
Stroke is one of the leading causes of mortality, with a high incidence of severe morbidity in survivors. The treatment to minimize tissue injury after stroke is still unsatisfactory and it is mandatory to develop effective treatment strategies for stroke. The pathophysiology of ischemic stroke is complex and involves many processes including energy failure, loss of ion homeostasis, increased intracellular calcium level, platelet aggregation, production of reactive oxygen species, disruption of blood brain barrier, and inflammation and leukocyte infiltration, etc. Tetrandrine, a bisbenzylisoquinoline alkaloid, has many pharmacologic effects including anti-inflammatory and cytoprotective effects. In addition, tetrandrine has been found to protect the liver, heart, small bowel and brain from ischemia/reperfusion injury. It is a calcium channel blocker, and can inhibit lipid peroxidation, reduce generation of reactive oxygen species, suppress the production of cytokines and inflammatory mediators, inhibit neutrophil recruitment and platelet aggregation, which are all devastating factors during ischemia/reperfusion injury of the brain. Because tetrandrine can counteract these important pathophysiological processes of ischemic stroke, it has the potential to be a protective agent for ischemic stroke.
Highlights
Introduction to Ischemic StrokeStroke is one of the leading causes of mortality, with a high incidence of severe morbidity in survivors [1]. 85% of all strokes are due to vascular occlusions, while 15% are primary intracerebral hemorrhage [1]
Leukocytes play an important role in mediating reperfusion-induced tissue injury and microvascular dysfunction because they accumulate in post-ischemic tissues prior to tissue injury, neutropenia decreases the injury response to ischemic stroke, and monoclonal antibodies against leukocyte or endothelial cell adhesion molecules protect against stroke injury [27]
Reports about the effects of tetrandrine on the stroke are limited; tetrandrine could protect the liver, heart, and small bowel from I/R injury, and, in addition, it counteracts some important pathophysiological processes of ischemic stroke as mentioned above, it has the potential to be a protective agent for ischemic stroke
Summary
Stroke is one of the leading causes of mortality, with a high incidence of severe morbidity in survivors [1]. 85% of all strokes are due to vascular occlusions (ischemic stroke), while 15% are primary intracerebral hemorrhage (hemorrhagic stroke) [1]. The majority of stroke patients show a slow evolution of brain injury that occurs over a period of hours-to-days following the attack [1] This period is the therapeutic window to inhibit the progression of tissue damage after ischemia and reperfusion; currently, few treatment options are available to minimize tissue death following a stroke [1,3]. The pathophysiology of stroke is complex and involves many processes, including energy failure, loss of ion homeostasis, acidosis, increased intracellular calcium levels, excitotoxicity, reactive oxygen species (ROS)-mediated toxicity, generation of arachidonic acid products, cytokine-mediated cytotoxicity, complement activation, disruption of blood-brain barrier, activation of glial cells, and inflammation and leukocyte infiltration [1] These are interrelated and coordinated events, which can lead to ischemic necrosis in the ischemic-core regions [1]. The treatment to minimize tissue injury after stroke is disappointing, it is mandatory to develop effective treatment strategies for stroke
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