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.
Malignant cerebral edema following cerebral infarction carries a high mortality rate, and its development involves two sequential phases: cytotoxic edema and vasogenic edema. According to the pathological timeline of post-ischemic brain edema, this review categorizes novel inflammatory biomarkers into five classes: upstream initiating signals, key molecules of the inflammasome and pyroptosis pathways, direct effectors of blood–brain barrier disruption and cerebral edema, brain tissue-specific structural injury markers, and novel acute-phase and immunoregulatory serum markers. The aim is to summarize the underlying molecular mechanisms and clinical relevance of these markers, thereby providing a reference for early intervention in post-infarction cerebral edema.