{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T15:15:45Z","timestamp":1784646945901,"version":"3.55.0"},"reference-count":58,"publisher":"MDPI AG","issue":"2","license":[{"start":{"date-parts":[[2014,2,12]],"date-time":"2014-02-12T00:00:00Z","timestamp":1392163200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>In the present work, we have studied whether cell death could be induced in cortical neurons from rats subjected to different period of O2 deprivation and low glucose (ODLG). This \u201cin vitro\u201d model is designed to emulate the penumbra area under ischemia. In these conditions, cortical neurons displayed loss of mitochondrial respiratory ability however, nor necrosis neither apoptosis occurred despite ROS production. The absence  of cellular death could be a consequence of increased antioxidant responses such as superoxide dismutase-1 (SOD1) and GPX3. In addition, the levels of reduced glutathione were augmented and HIF-1\/3\u03b1 overexpressed. After long periods of ODLG (12\u201324 h) cortical neurons showed cellular and mitochondrial membrane alterations and did not recuperate cellular viability during reperfusion. This could mean that therapies directed toward prevention of cellular and mitochondrial membrane imbalance or cell death through mechanisms other than necrosis or apoptosis, like authophagy, may be a way to prevent ODLG damage.<\/jats:p>","DOI":"10.3390\/ijms15022475","type":"journal-article","created":{"date-parts":[[2014,2,12]],"date-time":"2014-02-12T11:35:37Z","timestamp":1392204937000},"page":"2475-2493","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Antioxidant and Protective Mechanisms against Hypoxia and Hypoglycaemia in Cortical Neurons in Vitro"],"prefix":"10.3390","volume":"15","author":[{"given":"Jos\u00e9","family":"Merino","sequence":"first","affiliation":[{"name":"Departamento de Bioqu\u00edmica y Biolog\u00eda Molecular II, Facultad de Farmacia,  Universidad Complutense de Madrid (U.C.M.) Ciudad Universitaria, Madrid 28040, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00e9sar","family":"Roncero","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica y Biolog\u00eda Molecular II, Facultad de Farmacia,  Universidad Complutense de Madrid (U.C.M.) Ciudad Universitaria, Madrid 28040, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7223-0222","authenticated-orcid":false,"given":"Mar\u00eda","family":"Oset-Gasque","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica y Biolog\u00eda Molecular II, Facultad de Farmacia,  Universidad Complutense de Madrid (U.C.M.) Ciudad Universitaria, Madrid 28040, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmad","family":"Naddaf","sequence":"additional","affiliation":[{"name":"Faculty of Pharmacy, Isra University, PO Box 22, Amman 11622, Jordan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mar\u00eda","family":"Gonz\u00e1lez","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica y Biolog\u00eda Molecular II, Facultad de Farmacia,  Universidad Complutense de Madrid (U.C.M.) Ciudad Universitaria, Madrid 28040, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2014,2,12]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"399","DOI":"10.1038\/nrn1106","article-title":"Mechanism, challenges and opportunities in stroke","volume":"4","author":"Lo","year":"2003","journal-title":"Nat. Rev. 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