Neuroinflammation plays both beneficial and harmful roles in ischemic stroke. Following an ischemic stroke, secondary neuroinflammation can worsen injury but also aid in recovery. Proinflammatory signals from immune cells activate resident cells and recruit inflammatory cells like neutrophils, monocytes/macrophages, and T cells, exacerbating brain damage. The neurovascular unit, consisting of neurons, glia, vascular cells, and matrix components, is involved in the pathogenesis of stroke. Microglia, the resident immune cells of the brain, become activated after stroke, leading to the production of cytokines and MMPs that can compromise the blood-brain barrier (BBB). Activated microglia can cause neurotoxicity through the production of ROS, cytokines, and MMPs, but they also produce anti-inflammatory factors. Astrocytes, which are essential for maintaining the central nervous system, can become reactive after stroke, leading to the release of inflammatory factors and contributing to BBB disruption. Endothelial cells and pericytes are also involved in the BBB and play a role in the pathogenesis of stroke. Leukocytes, including neutrophils and T cells, infiltrate the ischemic area and contribute to secondary injury by releasing proinflammatory factors, ROS, and MMPs. The timing of immune cell entry into the ischemic area is critical, as it influences the severity of stroke outcomes. Cytokines and chemokines play a major role in the inflammatory response, with proinflammatory cytokines like IL-1β, TNF-α, and IL-6 contributing to brain damage. Chemokines, such as CCL-2 and CCR2, are involved in recruiting inflammatory cells and disrupting the BBB. Excitotoxicity, caused by the release of excitatory amino acids like glutamate, leads to neuronal damage. The balance between beneficial and harmful inflammatory responses is crucial for developing therapeutic strategies to combat ischemic stroke. Understanding the time-dependent role of inflammatory factors can help in developing new diagnostic, prognostic, and therapeutic neuroprotective strategies for post-stroke inflammation.Neuroinflammation plays both beneficial and harmful roles in ischemic stroke. Following an ischemic stroke, secondary neuroinflammation can worsen injury but also aid in recovery. Proinflammatory signals from immune cells activate resident cells and recruit inflammatory cells like neutrophils, monocytes/macrophages, and T cells, exacerbating brain damage. The neurovascular unit, consisting of neurons, glia, vascular cells, and matrix components, is involved in the pathogenesis of stroke. Microglia, the resident immune cells of the brain, become activated after stroke, leading to the production of cytokines and MMPs that can compromise the blood-brain barrier (BBB). Activated microglia can cause neurotoxicity through the production of ROS, cytokines, and MMPs, but they also produce anti-inflammatory factors. Astrocytes, which are essential for maintaining the central nervous system, can become reactive after stroke, leading to the release of inflammatory factors and contributing to BBB disruption. Endothelial cells and pericytes are also involved in the BBB and play a role in the pathogenesis of stroke. Leukocytes, including neutrophils and T cells, infiltrate the ischemic area and contribute to secondary injury by releasing proinflammatory factors, ROS, and MMPs. The timing of immune cell entry into the ischemic area is critical, as it influences the severity of stroke outcomes. Cytokines and chemokines play a major role in the inflammatory response, with proinflammatory cytokines like IL-1β, TNF-α, and IL-6 contributing to brain damage. Chemokines, such as CCL-2 and CCR2, are involved in recruiting inflammatory cells and disrupting the BBB. Excitotoxicity, caused by the release of excitatory amino acids like glutamate, leads to neuronal damage. The balance between beneficial and harmful inflammatory responses is crucial for developing therapeutic strategies to combat ischemic stroke. Understanding the time-dependent role of inflammatory factors can help in developing new diagnostic, prognostic, and therapeutic neuroprotective strategies for post-stroke inflammation.