Acute ischemic stroke is the third leading cause of death in industrialized countries and the most common cause of permanent disability in adults. Despite advances in understanding the pathophysiology of cerebral ischemia, therapeutic options remain limited. Only recombinant tissue plasminogen activator (rt-PA) is currently approved for thrombolysis in acute ischemic stroke. However, its use is limited by a short therapeutic window, risk of hemorrhage, and reperfusion injury. Two key mechanisms involved in ischemic stroke are oxidative stress and inflammation. Brain tissue lacks sufficient antioxidant defenses, leading to oxidative damage and inflammation. This review discusses the molecular aspects of oxidative stress and inflammation in ischemic stroke and potential therapeutic strategies targeting neuroinflammation and the innate immune system. Recent studies suggest that regulatory T cells may offer novel neuroprotective therapies. The ischemic cascade involves a series of biochemical events leading to cell death. Oxidative stress contributes to ischemic injury, and Nrf2 is a key transcription factor regulating antioxidant genes. Ischemia/reperfusion injury leads to secondary damage, with inflammation playing a critical role. Post-ischemic inflammation involves microglia and astrocytes, which release cytokines and contribute to neuronal cell death. Cytokines such as TNF-α and IL-1β exacerbate cerebral injury, while IL-10 may be neuroprotective. Chemokines and cell adhesion molecules also play roles in inflammation. Matrix metalloproteinases contribute to blood-brain barrier disruption. Regulatory T cells may prevent secondary infarct growth by modulating inflammation. Post-stroke recovery involves brain plasticity and neurogenesis. Despite advances, effective neuroprotective therapies remain limited. rt-PA remains the only approved treatment, but its limitations highlight the need for new approaches targeting inflammation and immune responses.Acute ischemic stroke is the third leading cause of death in industrialized countries and the most common cause of permanent disability in adults. Despite advances in understanding the pathophysiology of cerebral ischemia, therapeutic options remain limited. Only recombinant tissue plasminogen activator (rt-PA) is currently approved for thrombolysis in acute ischemic stroke. However, its use is limited by a short therapeutic window, risk of hemorrhage, and reperfusion injury. Two key mechanisms involved in ischemic stroke are oxidative stress and inflammation. Brain tissue lacks sufficient antioxidant defenses, leading to oxidative damage and inflammation. This review discusses the molecular aspects of oxidative stress and inflammation in ischemic stroke and potential therapeutic strategies targeting neuroinflammation and the innate immune system. Recent studies suggest that regulatory T cells may offer novel neuroprotective therapies. The ischemic cascade involves a series of biochemical events leading to cell death. Oxidative stress contributes to ischemic injury, and Nrf2 is a key transcription factor regulating antioxidant genes. Ischemia/reperfusion injury leads to secondary damage, with inflammation playing a critical role. Post-ischemic inflammation involves microglia and astrocytes, which release cytokines and contribute to neuronal cell death. Cytokines such as TNF-α and IL-1β exacerbate cerebral injury, while IL-10 may be neuroprotective. Chemokines and cell adhesion molecules also play roles in inflammation. Matrix metalloproteinases contribute to blood-brain barrier disruption. Regulatory T cells may prevent secondary infarct growth by modulating inflammation. Post-stroke recovery involves brain plasticity and neurogenesis. Despite advances, effective neuroprotective therapies remain limited. rt-PA remains the only approved treatment, but its limitations highlight the need for new approaches targeting inflammation and immune responses.