Inflammatory mediators play a crucial role in stroke pathophysiology, offering new therapeutic opportunities. Brain cells can produce cytokines and chemokines, and express adhesion molecules, leading to an inflammatory response after injury. Neutrophil accumulation early after stroke is believed to contribute to brain tissue loss, and studies have shown that neutrophil depletion reduces this effect. Inflammation is a rapid and dynamic process that contributes to tissue injury, but cytokines may also provide neuroprotection by promoting repair and recovery. However, the complex interplay between inflammatory and protective processes requires further research to develop effective therapies. Stroke is a leading cause of death and disability, with limited treatment options beyond tissue plasminogen activator (tPA). Stroke therapies are in high demand, with significant economic and health care costs. Stroke causes brain injury through ischemia, leading to reduced energy availability and cellular dysfunction. This results in increased intracellular calcium, which triggers a cascade of events leading to neuronal death, including excitotoxicity, free radical damage, and breakdown of cellular structures. Previous therapeutic approaches targeting calcium channels, glutamate receptors, and free radicals have been largely unsuccessful due to the rapid onset of these processes after stroke, making it difficult to intervene effectively. The brain's inflammatory response to injury, involving cytokines, chemokines, and adhesion molecules, presents a promising therapeutic target. Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) are key inflammatory mediators involved in stroke pathophysiology. They can both contribute to tissue damage and promote neuroprotection, depending on the context. TNF-α and IL-1β are involved in the early inflammatory response to stroke, with their expression peaking within hours of injury. These cytokines can enhance leukocyte adhesion and infiltration, contributing to tissue damage. However, they may also play a protective role by promoting repair and regeneration. The expression of these cytokines is tightly regulated, and their modulation may offer therapeutic benefits. Recent research has focused on targeting cytokines and inflammatory pathways to develop novel therapies. Inhibitors of the mitogen-activated protein kinase (MAPK) cascade, particularly p38 MAPK, have shown promise in blocking inflammatory cytokine production and apoptosis. These inhibitors can prevent the activation of downstream signaling pathways that contribute to neuronal injury. In conclusion, the inflammatory response to stroke is a complex and dynamic process that can both damage and protect the brain. Understanding the role of inflammatory mediators and their regulation is essential for developing effective therapies. Targeting cytokines, adhesion molecules, and inflammatory pathways offers new opportunities for neuroprotection and recovery after stroke.Inflammatory mediators play a crucial role in stroke pathophysiology, offering new therapeutic opportunities. Brain cells can produce cytokines and chemokines, and express adhesion molecules, leading to an inflammatory response after injury. Neutrophil accumulation early after stroke is believed to contribute to brain tissue loss, and studies have shown that neutrophil depletion reduces this effect. Inflammation is a rapid and dynamic process that contributes to tissue injury, but cytokines may also provide neuroprotection by promoting repair and recovery. However, the complex interplay between inflammatory and protective processes requires further research to develop effective therapies. Stroke is a leading cause of death and disability, with limited treatment options beyond tissue plasminogen activator (tPA). Stroke therapies are in high demand, with significant economic and health care costs. Stroke causes brain injury through ischemia, leading to reduced energy availability and cellular dysfunction. This results in increased intracellular calcium, which triggers a cascade of events leading to neuronal death, including excitotoxicity, free radical damage, and breakdown of cellular structures. Previous therapeutic approaches targeting calcium channels, glutamate receptors, and free radicals have been largely unsuccessful due to the rapid onset of these processes after stroke, making it difficult to intervene effectively. The brain's inflammatory response to injury, involving cytokines, chemokines, and adhesion molecules, presents a promising therapeutic target. Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) are key inflammatory mediators involved in stroke pathophysiology. They can both contribute to tissue damage and promote neuroprotection, depending on the context. TNF-α and IL-1β are involved in the early inflammatory response to stroke, with their expression peaking within hours of injury. These cytokines can enhance leukocyte adhesion and infiltration, contributing to tissue damage. However, they may also play a protective role by promoting repair and regeneration. The expression of these cytokines is tightly regulated, and their modulation may offer therapeutic benefits. Recent research has focused on targeting cytokines and inflammatory pathways to develop novel therapies. Inhibitors of the mitogen-activated protein kinase (MAPK) cascade, particularly p38 MAPK, have shown promise in blocking inflammatory cytokine production and apoptosis. These inhibitors can prevent the activation of downstream signaling pathways that contribute to neuronal injury. In conclusion, the inflammatory response to stroke is a complex and dynamic process that can both damage and protect the brain. Understanding the role of inflammatory mediators and their regulation is essential for developing effective therapies. Targeting cytokines, adhesion molecules, and inflammatory pathways offers new opportunities for neuroprotection and recovery after stroke.