{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:36:45Z","timestamp":1777793805680,"version":"3.51.4"},"reference-count":38,"publisher":"SAGE Publications","issue":"10","license":[{"start":{"date-parts":[[2011,5,18]],"date-time":"2011-05-18T00:00:00Z","timestamp":1305676800000},"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":[[2011,10]]},"abstract":"<jats:p>\n                    The aim of this study was to evaluate the long-term effects of lithium treatment on neonatal hypoxic-ischemic brain injury, inflammation, and neural stem\/progenitor cell (NSPC) proliferation and survival. Nine-day-old male rats were subjected to unilateral hypoxia\u2013ischemia (HI) and 2 mmol\/kg lithium chloride was injected intraperitoneally immediately after the insult. Additional lithium injections, 1 mmol\/kg, were administered at 24-hour intervals for 7 days. Animals were killed 6, 24, 72 hours, or 7 weeks after HI. Lithium reduced total tissue loss by 69%, from 89.4\u00b114.6 mm\n                    <jats:sup>3<\/jats:sup>\n                    in controls ( n = 15) to 27.6 \u00b16.2 mm\n                    <jats:sup>3<\/jats:sup>\n                    in lithium-treated animals ( n = 14) 7 weeks after HI ( P&lt;0.001). Microglia activation was inhibited by lithium treatment, as judged by Iba-1 and galectin-3 immunostaining, and reduced interleukin-1\u03b2 and CCL2 levels. Lithium increased progenitor, rather than stem cell, proliferation in both nonischemic and ischemic brains, as judged by 5-bromo-2-deoxyuridine labeling 24 and 72 hours as well as by phospho-histone H3 and brain lipid-binding protein labeling 7 weeks after HI. Lithium treatment also promoted survival of newborn NSPCs, without altering the relative levels of neuronal and astroglial differentiation. In summary, lithium conferred impressive, morphological long-term protection against neonatal HI, at least partly by inhibiting inflammation and promoting NSPC proliferation and survival.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.2011.75","type":"journal-article","created":{"date-parts":[[2011,5,18]],"date-time":"2011-05-18T04:22:14Z","timestamp":1305692534000},"page":"2106-2115","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":92,"title":["Lithium-Mediated Long-Term Neuroprotection in Neonatal Rat Hypoxia\u2013Ischemia is Associated with Antiinflammatory Effects and Enhanced Proliferation and Survival of Neural Stem\/Progenitor Cells"],"prefix":"10.1177","volume":"31","author":[{"given":"Hongfu","family":"Li","sequence":"first","affiliation":[{"name":"Center for Brain Repair and Rehabilitation, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden"},{"name":"Department of 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