Obiective To establish hypoxia damage model of neural stem cells (NSCs) and investigate the protection of lithium on them through culture NSCs. Methods NSCs were cultured from neonatal mice,immunocytochemistry was used to examine the Nestin expression of NSC,the forth passage cells were divided into control,hypoxia and lithium groups,NSE and GFAP were used to evaluate cell differentiation,cck-8 was used to evaluate cell proliferation,and NSE and GFAP were used to evaluate cell differentiation. Result NSCs under hypoxia 95%N2,5%CO2 for 30 minutes could establish hypoxia damage model in vitro and certain concentration of lithium protected the damages. Conclusion Lithium can protect NSCs under hypoxia and may prevent NSCs against hypoxia injury.
Key words
neural stem cells /
hypoxia /
lithium
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
References
[1] Pisani F,Orsini M,Braibani S,et al.Development of epilepsyin new-borns with moderate hypoxic-ischemic encephalopathy and neonatal seizures[J].Brain Dev,2009,31(1):64-68.
[2] 邵肖梅,叶鸿瑁,丘小汕.实用新生儿学[M].4版.2011:700-705.
[3] Li HF,Li Q,Du XN,et al.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[J].Journal of Cerebral Blood Flow & Metabolism,2011,31(10):2106-2115.
[4] 王钰,尹晓娟.锂对新生儿缺血缺氧性脑损伤神经保护作用的研究进展[J].中国儿童保健杂志,2011,19(11):1002-1003.
[5] 龚敏,李树清.体外培养细胞缺氧模型及特点[J].临床合理用药,2011,4(1):157-158.
[6] Tutunculer E.The prolecfive role of melalonin in experimental hypoxic brain damage[J].Pediatr Int,2005,47(4):434-439.
[7] Romanko MJ,Rothstein RP.Levis on SW Neural stem cells in the subventricular zone are resiIient to hypoxia / ischemia whereas progenitorsare vulnerable[J].J Cereb Blood Flow Metab,2004,24(7):814-825.
[8] Brazel CY,Rosti RT,Boyce S,et al.Perinatal hypoxia-ischemia damages and depletes progenitors from the mouse subventricular zone[J].Dev Neurosci,2004,26(2-4):266-274.
[9] Acker T,Acker H.Cellular oxygen sensing need in CNS function:physiological and pathological implications[J].JEXP Biol,2004,207(18):3171-3188. [10] Bian Q,Shi T,Chuang DM,et al.Lithium reduces ischemia-induced hippocampal CA1 damage and behavioral deficits in gerbils[J].Brain Res,2007,1184:270-276.
[11] Xia Y,Wang CZ,Liu J,et al.Lithium protection of phencyclidine-induced neurotoxicity in developing brain:the role of phosphatidylinositol-3 kinase/Akt and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling pathways[J].J Pharmacol Exp Ther,2008,326:838-848.
[12] Crespo-Biel N,Camins A,Pallas M,et al.Evidence of calpain/cdk5 pathway inhibition by lithium in 3-nitropropionic acid toxicity in vivo and in vitro[J].Neuropharmacology,2009,56:422-428.
[13] Jin SK,Mi-Yoon C,In Tag Y,et al.Lithium selectively increases neuronal differentiation of hippocampal neural progenitor cells both in vitro and in vivo[J].Journal of Neurochemistry,2004,89:324-336.
PDF(593 KB)
