Abstract
Acute ischemic stroke is the third leading cause of death in industrialized countries and the most frequent cause of permanent disability in adults worldwide. Despite advances in the understanding of the pathophysiology of cerebral ischemia, therapeutic options remain limited. Only recombinant tissue-plasminogen activator (rt-PA) for thrombolysis is currently approved for use in the treatment of this devastating disease. However, its use is limited by its short therapeutic window (three hours), complications derived essentially from the risk of hemorrhage, and the potential damage from reperfusion/ischemic injury. Two important pathophysiological mechanisms involved during ischemic stroke are oxidative stress and inflammation. Brain tissue is not well equipped with antioxidant defenses, so reactive oxygen species and other free radicals/oxidants, released by inflammatory cells, threaten tissue viability in the vicinity of the ischemic core. This review will discuss the molecular aspects of oxidative stress and inflammation in ischemic stroke and potential therapeutic strategies that target neuroinflammation and the innate immune system. Currently, little is known about endogenous counterregulatory immune mechanisms. However, recent studies showing that regulatory T cells are major cerebroprotective immunomodulators after stroke suggest that targeting the endogenous adaptive immune response may offer novel promising neuroprotectant therapies.
Highlights
Stroke is the third leading cause of death in industrialized countries [1] and the most frequent cause of permanent disability in adults worldwide [2]
In the Western world, over 70% of individuals experiencing a stroke are over 65 years of age
The most common cause of stroke is the sudden occlusion of a blood vessel by a thrombus or embolism, resulting in an almost immediate loss of oxygen and glucose to the cerebral tissue
Summary
Stroke is the third leading cause of death in industrialized countries [1] and the most frequent cause of permanent disability in adults worldwide [2]. An adequate adaptive immune response after acute brain ischemia plays an important role in response to ischemic injury as shown by the tremendous potential of Treg cells to prevent secondary infarct growth by counteracting the production of proinflammatory cytokines and by modulating the activation of lymphocytes and microglia in the ischemic brain [57]. These results provide new insights into the immunopathogenesis of acute ischemic stroke and could lead to new approaches that involve immune modulation using Treg cells. Because of these drawbacks the optimum treatment of cerebral focal ischemia remains one of the major challenges in clinical medicine
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