Pathophysiological process of neuroinflammatory response after ischemic stroke. After ischemic brain injury, DAMPs are released during cell ischemia, hypoxia, and necrosis, promoting the activation of microglia, astrocytes, brain endothelial cells, and perivascular immune cells. Microglia polarize into classical (M1) or alternative (M2) microglia and secrete proinflammatory cytokines, anti-inflammatory cytokines, adhesion molecules, and chemokines. Activated astrocytes initially secrete proinflammatory cytokines, followed by anti-inflammatory cytokines, chemokines, and adhesion molecules. Proinflammatory cytokines contribute to the BBB breakdown and exacerbate the inflammatory response, while anti-inflammatory cytokines counteract this process and play a neuroprotective role. Adhesion molecules and chemokines facilitate the infiltration of peripheral immune cells into the BBB and promote the inflammatory response. DAMPs, damage-associated molecular patterns; BBB, blood-brain barrier; TLRs, Toll-like receptors; M1, classical microglia; M2, alternative microglia.