{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T14:16:39Z","timestamp":1761488199328},"reference-count":69,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2009,2,17]],"date-time":"2009-02-17T00:00:00Z","timestamp":1234828800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2009,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Developing oligodendrocytes (pre\u2010OLs) are highly vulnerable to hypoxic\u2010ischemic injury and associated excitotoxicity and oxidative stress. 17\u03b2\u2010Estradiol plays an important role in the development and function of the CNS and is neuroprotective. The sudden drop in circulating estrogen after birth may enhance the susceptibility of developing OLs to injury. Estrogen receptor (ER)\u2013\u03b1 and ER\u2010\u03b2 are both expressed in OLs. We examined the effect of 17\u03b2\u2010estradiol on oxygen\u2010glucose deprivation and oxidative stress\u2013induced cell death in rat pre\u2010OLs in vitro and on hypoxic\u2010ischemic brain injury in vivo. Pre\u2010OLs in culture were subjected to oxygen\u2010glucose deprivation (OGD) or glutathione depletion in the presence or absence of 17\u03b2\u2010estradiol. LDH release, the Alamar blue assay, and phase\u2010contrast microscopy were used to assess cell viability. Hypoxic\u2010ischemic injury was generated in 6\u2010day\u2010old rats (P6) by unilateral carotid ligation and hypoxia (6% O<jats:sub>2<\/jats:sub> for 1 hr). Rat pups received one intraperitoneal injection of 300 or 600 \u03bcg\/kg 17\u03b2\u2010estradiol or vehicle 12 hr prior to the surgical procedure. Injury was assessed by myelin basic protein (MBP) immunocytochemistry at P10. 17\u03b2\u2010Estradiol produced significant protection against OGD\u2010induced cell death in primary OLs (EC<jats:sub>50<\/jats:sub> = 1.3 \u00b1 0.46 \u00d7 10<jats:sup>\u22129<\/jats:sup> M) and against oxidative stress. Moreover, 17\u03b2\u2010estradiol attenuated the loss of MBP labeling in P10 pups ipsilateral to the carotid ligation. These results suggest a potential role for estrogens in attenuation of hypoxic\u2010ischemic and oxidative injury to developing OLs and in the prevention of periventricular leukomalacia. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22023","type":"journal-article","created":{"date-parts":[[2009,2,17]],"date-time":"2009-02-17T18:12:28Z","timestamp":1234894348000},"page":"2078-2086","source":"Crossref","is-referenced-by-count":69,"title":["17\u03b2\u2010estradiol protects against hypoxic\/ischemic white matter damage in the neonatal rat brain"],"prefix":"10.1002","volume":"87","author":[{"given":"Bettina","family":"Gerstner","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joan","family":"Lee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tara 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