{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:55:52Z","timestamp":1786978552826,"version":"build-2736575974"},"reference-count":52,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2023,5,17]],"date-time":"2023-05-17T00:00:00Z","timestamp":1684281600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2023,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Cerebral ischemia\/reperfusion (I\/R) injury remains a grievous health threat, and herein effective therapy is urgently needed. This study explored the protection of neuroglobin (Ngb) in rats with cerebral I\/R injury. The focal cerebral I\/R rat models were established by middle cerebral artery occlusion (MCAO) and neuronal injury models were established by oxygen\u2013glucose deprivation\/reoxygenation (OGD\/R) treatment. The brain injury of rats was assessed. Levels of Ngb, Bcl\u20102, Bax, endoplasmic reticulum stress (ERS)\u2010related markers, and Syt1 were measured by immunofluorescence staining and Western blotting. The cytotoxicity in neurons was assessed by lactate dehydrogenase (LDH) release assay. Levels of intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and mitochondrial function\u2010related indicators were determined. The binding between Ngb and Syt1 was detected by co\u2010immunoprecipitation. Ngb was upregulated in cerebral I\/R rats and its overexpression alleviated brain injury. In OGD\/R\u2010induced neurons, Ngb overexpression decreased LDH level and neuronal apoptosis, decreased Ca\n                    <jats:sup>2+<\/jats:sup>\n                    content, and mitigated mitochondrial dysfunction and ERS\u2010related apoptosis. However, Ngb silencing imposed the opposite effects. Importantly, Ngb could bind to Syt1. Syt1 knockdown partially counteracted the alleviation of Ngb on OGD\/R\u2010induced injury in neurons and cerebral I\/R injury in rats. Briefly, Ngb extenuated cerebral I\/R injury by repressing mitochondrial dysfunction and endoplasmic reticulum stress\u2010mediated neuronal apoptosis through Syt1.\n                  <\/jats:p>","DOI":"10.1002\/tox.23815","type":"journal-article","created":{"date-parts":[[2023,5,17]],"date-time":"2023-05-17T13:09:43Z","timestamp":1684328983000},"page":"1891-1904","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Neuroglobin protects against cerebral ischemia\/reperfusion injury in rats by suppressing mitochondrial dysfunction and endoplasmic reticulum stress\u2010mediated neuronal apoptosis through synaptotagmin\u20101"],"prefix":"10.1002","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5680-9202","authenticated-orcid":false,"given":"Lihong","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Neurointervention and Neurocritical Care Dalian Central Hospital Affiliated to Dalian 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