{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:50:21Z","timestamp":1777794621509,"version":"3.51.4"},"reference-count":36,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2022,12,22]],"date-time":"2022-12-22T00:00:00Z","timestamp":1671667200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2023,4]]},"abstract":"<jats:p>\n                    Cerebral ischemia triggers inflammatory changes, and early complications and unfavorable outcomes of endovascular thrombectomy for brain occlusion promote the recruitment of various cell types to the ischemic area. Although anti-inflammatory M2-type macrophages are thought to exert protective effects against cerebral ischemia, little has been clarified regarding the significance of post-ischemic phase-dependent modulation of M2-type macrophages. To test our hypothesis that post-ischemic phase-dependent modulation of macrophages represents a potential therapy against ischemic brain damage, the effects on rats of an M2-type macrophage-specific activator, Gc-protein macrophage-activating factor (GcMAF), were compared with vehicle-treated control rats in the acute (day 0\u20136) or subacute (day 7\u201313) phase after ischemia induction. Acute-phase GcMAF treatment augmented both anti-inflammatory CD163\n                    <jats:sup>+<\/jats:sup>\n                    M2-type- and pro-inflammatory CD16\n                    <jats:sup>+<\/jats:sup>\n                    M1-type macrophages, resulting in no beneficial effects. Conversely, subacute-phase GcMAF injection increased only CD163\n                    <jats:sup>+<\/jats:sup>\n                    M2-type macrophages accompanied by elevated mRNA levels of arginase-1 and interleukin-4. M2-type macrophages co-localized with CD36\n                    <jats:sup>+<\/jats:sup>\n                    phagocytic cells led to clearance of the infarct area, which were abrogated by clodronate-liposomes. Expression of survival-related molecules on day 28 at the infarct border was augmented by GcMAF. These data provide new and important insights into the significance of M2-type macrophage-specific activation as post-ischemic phase-dependent therapy.\n                  <\/jats:p>","DOI":"10.1177\/0271678x221147090","type":"journal-article","created":{"date-parts":[[2022,12,22]],"date-time":"2022-12-22T03:38:50Z","timestamp":1671680330000},"page":"531-541","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":3,"title":["Role of post-ischemic phase-dependent modulation of anti-inflammatory M2-type macrophages against rat brain damage"],"prefix":"10.1177","volume":"43","author":[{"given":"Yoshitaka","family":"Kurashiki","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroshi","family":"Kagusa","sequence":"additional","affiliation":[{"name":"Department of 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