This article reviews the inflammatory mechanisms involved in ischemic stroke and discusses potential therapeutic strategies targeting neuroinflammation and the innate immune system. Acute ischemic stroke is a leading cause of death and disability, with limited therapeutic options beyond recombinant tissue-plasminogen activator (rt-PA) for thrombolysis. Oxidative stress and inflammation are key pathophysiological mechanisms in ischemic stroke, contributing to neuronal injury and tissue damage. The review highlights the role of reactive oxygen species, free radicals, and other oxidants released by inflammatory cells in damaging brain tissue. It also explores the potential of regulatory T cells as cerebroprotective immunomodulators and the therapeutic promise of targeting endogenous adaptive immune responses. Additionally, the article discusses the ischemic cascade, hyperbaric and normobaric oxygen therapies, and the involvement of cytokines, chemokines, cellular adhesion molecules, matrix metalloproteinases, and regulatory T lymphocytes in post-ischemic inflammation. The authors conclude by emphasizing the need for further research to develop effective treatments for ischemic stroke, particularly those that can modulate the immune response to reduce secondary damage and improve patient outcomes.This article reviews the inflammatory mechanisms involved in ischemic stroke and discusses potential therapeutic strategies targeting neuroinflammation and the innate immune system. Acute ischemic stroke is a leading cause of death and disability, with limited therapeutic options beyond recombinant tissue-plasminogen activator (rt-PA) for thrombolysis. Oxidative stress and inflammation are key pathophysiological mechanisms in ischemic stroke, contributing to neuronal injury and tissue damage. The review highlights the role of reactive oxygen species, free radicals, and other oxidants released by inflammatory cells in damaging brain tissue. It also explores the potential of regulatory T cells as cerebroprotective immunomodulators and the therapeutic promise of targeting endogenous adaptive immune responses. Additionally, the article discusses the ischemic cascade, hyperbaric and normobaric oxygen therapies, and the involvement of cytokines, chemokines, cellular adhesion molecules, matrix metalloproteinases, and regulatory T lymphocytes in post-ischemic inflammation. The authors conclude by emphasizing the need for further research to develop effective treatments for ischemic stroke, particularly those that can modulate the immune response to reduce secondary damage and improve patient outcomes.