{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T19:30:41Z","timestamp":1785526241536,"version":"3.56.0"},"reference-count":37,"publisher":"Portland Press Ltd.","issue":"17","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2016,9,1]]},"abstract":"<jats:p>The major ghrelin forms, acylated ghrelin and des-acylated ghrelin, are novel gastrointestinal hormones. Moreover, emerging evidence indicates that these peptides may have other functions including neuro- and vaso-protection. Here, we investigated whether post-stroke treatment with acylated ghrelin or des-acylated ghrelin could improve functional and histological endpoints of stroke outcome in mice after transient middle cerebral artery occlusion (tMCAo). We found that des-acylated ghrelin (1\u00a0mg\/kg) improved neurological and functional performance, reduced infarct and swelling, and decreased apoptosis. In addition, it reduced blood-brain barrier (BBB) disruption in\u00a0vivo and attenuated the hyper-permeability of mouse cerebral microvascular endothelial cells after oxygen glucose deprivation and reoxygenation (OGD + RO). By contrast, acylated ghrelin (1\u00a0mg\/kg or 5\u00a0mg\/kg) had no significant effect on these endpoints of stroke outcome. Next we found that des-acylated ghrelin's vasoprotective actions were associated with increased expression of tight junction proteins (occludin and claudin-5), and decreased cell death. Moreover, it attenuated superoxide production, Nox activity and expression of 3-nitrotyrosine. Collectively, these results demonstrate that post-stroke treatment with des-acylated ghrelin, but not acylated ghrelin, protects against ischaemia\/reperfusion-induced brain injury and swelling, and BBB disruption, by reducing oxidative and\/or nitrosative damage.<\/jats:p>","DOI":"10.1042\/cs20160077","type":"journal-article","created":{"date-parts":[[2016,6,15]],"date-time":"2016-06-15T13:04:00Z","timestamp":1465995840000},"page":"1545-1558","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Protective actions of des-acylated ghrelin on brain injury and blood\u2013brain barrier disruption after stroke in mice"],"prefix":"10.1042","volume":"130","author":[{"given":"Jacqueline\u00a0M.","family":"Ku","sequence":"first","affiliation":[{"name":"Cerebrovascular and Stroke Laboratory, School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria 3083, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammadali","family":"Taher","sequence":"additional","affiliation":[{"name":"Cerebrovascular and Stroke Laboratory, School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria 3083, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai\u00a0Yee","family":"Chin","sequence":"additional","affiliation":[{"name":"Cerebrovascular and Stroke Laboratory, School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria 3083, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tom","family":"Barsby","sequence":"additional","affiliation":[{"name":"Cerebrovascular and Stroke Laboratory, School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria 3083, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victoria","family":"Austin","sequence":"additional","affiliation":[{"name":"Cerebrovascular and Stroke Laboratory, School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria 3083, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Connie\u00a0H.Y.","family":"Wong","sequence":"additional","affiliation":[{"name":"Centre for Inflammatory Diseases, Department of Medicine, Monash Medical Centre, Monash University, Melbourne, Victoria 3168, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zane\u00a0B.","family":"Andrews","sequence":"additional","affiliation":[{"name":"Department of Physiology, Monash University, Melbourne, Victoria 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah\u00a0J.","family":"Spencer","sequence":"additional","affiliation":[{"name":"Cerebrovascular and Stroke Laboratory, School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria 3083, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alyson\u00a0A.","family":"Miller","sequence":"additional","affiliation":[{"name":"Cerebrovascular and Stroke Laboratory, School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria 3083, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2016,7,26]]},"reference":[{"key":"2021113010421500700_B1","doi-asserted-by":"publisher","first-page":"796","DOI":"10.1038\/nm.2399","article-title":"The immunology of stroke: from mechanisms to translation","volume":"17","author":"Iadecola","year":"2011","journal-title":"Nat. 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