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Lithium-mediated long-term neuroprotection in neonatal rat hypoxia-ischemia is associated with antiinflammatory effects and enhanced proliferation and survival of neural stem/progenitor cells.

Artikel i vetenskaplig tidskrift
Författare Hongfu Li
Qian Li
Xiaonan Du
Yanyan Sun
Xiaoyang Wang
Guido Kroemer
Klas Blomgren
Changlian Zhu
Publicerad i Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
Volym 31
Nummer/häfte 10
Sidor 2106–2115
ISSN 1559-7016
Publiceringsår 2011
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Sidor 2106–2115
Språk en
Länkar dx.doi.org/10.1038/jcbfm.2011.75
Ämnesord asphyxia; inflammation; microglia; neurogenesis; stem cell
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

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-ischemia (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±14.6 mm(3) in controls (n=15) to 27.6±6.2 mm(3) in lithium-treated animals (n=14) 7 weeks after HI (P<0.001). Microglia activation was inhibited by lithium treatment, as judged by Iba-1 and galectin-3 immunostaining, and reduced interleukin-1β 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.Journal of Cerebral Blood Flow & Metabolism advance online publication, 18 May 2011; doi:10.1038/jcbfm.2011.75.

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