Ischemic stroke (IS) is one of the important diseases threatening human health. The occurrence and development of IS can trigger a series of complex pathophysiological changes, including damage to the blood-brain barrier, ion imbalance, oxidative stress, mitochondrial damage, which ultimately lead to the apoptosis and necrosis of nerve cells in the ischemic area. Impaired blood-brain barrier is a key factor for cerebral edema, hemorrhagic transformation and poor prognosis in patients with IS, and neuroinflammatory response plays an important role in the damage and repair of the blood-brain barrier. This article mainly focuses on the neuroinflammatory response mediated by glial cells, pro-inflammatory cytokines and matrix metalloproteinases and the related mechanisms of IS blood-brain barrier damage and repair, in order to provide new directions for the treatment of IS.