{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T01:40:41Z","timestamp":1792719641858,"version":"4.5.0"},"reference-count":40,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2009,12,2]],"date-time":"2009-12-02T00:00:00Z","timestamp":1259712000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2010,3]]},"abstract":"<jats:p>Cerebral ischemia-elicited inflammatory responses are driven by inflammatory mediators produced both by central (e.g., neurons and microglia) and infiltrating peripheral immune cells (e.g., macrophage\/monocyte), and contribute to the evolution of tissue injury. A ubiquitous molecule, spermine, is released from injured cells, and counter-regulates release of various proinflammatory cytokines. However, the spermine-mediated anti-inflammatory activities are dependent on the availability of fetuin-A, a liver-derived negative acute-phase protein. Using an animal model of focal cerebral ischemia (i.e., permanent middle cerebral artery occlusion, MCAo), we found that levels of fetuin-A in the ischemic brain tissue were elevated in a time-dependent manner, starting between 2 and 6 h, peaking around 24 to 48 h, and returning to baseline 72 h after MCAo. When administered peripherally, exogenous fetuin-A gained entry across the BBB into the ischemic brain tissue, and dose dependently reduced brain infarct volume at 24 h after MCAo. Meanwhile, fetuin-A effectively attenuated (i) ischemia-induced HMGB1 depletion from the ischemic core; (ii) activation of centrally (e.g., microglia) and peripherally derived immune cells (e.g., macrophage\/monocytes); and (iii) TNF production in ischemic brain tissue. Taken together, these experimental data suggest that fetuin-A protects against early cerebral ischemic injury partly by attenuating the brain inflammatory response.<\/jats:p>","DOI":"10.1038\/jcbfm.2009.247","type":"journal-article","created":{"date-parts":[[2009,12,2]],"date-time":"2009-12-02T04:01:16Z","timestamp":1259726476000},"page":"493-504","source":"Crossref","is-referenced-by-count":70,"title":["Peripheral Administration of Fetuin-A Attenuates Early Cerebral Ischemic Injury in Rats"],"prefix":"10.1177","volume":"30","author":[{"given":"Haichao","family":"Wang","sequence":"first","affiliation":[{"name":"The Feinstein Institute for Medical Research, Manhasset, New York, USA"},{"name":"Department of Emergency Medicine, North Shore University Hospital\u2014New York University School of Medicine, Manhasset, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Emergency 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