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锂的神经元保护作用及对铅神经毒性的拮抗效应

Neuroprotection of lithium and the antegonism of lithium to toxic effects of lead on primary culturing cerebrocortical neurons in vitro
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摘要 目的 探讨铅的神经毒性、锂的神经元保护作用以及锂对铅神经毒性的拮抗效应 ,研究不同浓度氯化锂和醋酸铅对原代培养皮层神经元生长及存活的影响。方法 建立新生大鼠皮层神经元原代培养技术 ,通过加入不同浓度氯化锂、醋酸铅及同时加入 5mmol L的氯化锂和不同浓度醋酸铅 ,显微镜下观察神经细胞的生长和存活情况 ,目镜测量神经元突起长度 ,噻唑蓝 (MTT)还原法检测细胞生长活力。结果 各浓度氯化锂均可促进神经元突起生长 (P <0 0 5 ) ,1 2 5mmol L以上浓度的氯化锂可使神经元生长活力降低 (P <0 0 5 ) ;醋酸铅 (≥ 10 - 7mol L)能抑制神经元生长 ,其神经元突起长度明显短于对照组 (P <0 0 1) ,各浓度的醋酸铅均可使神经元生长活力降低 (P <0 0 1) ;5mmol L浓度的锂对染铅神经元有明显的保护作用和促生长作用 ,表现为铅浓度为 10 - 6 mol L与 10 - 5mmol L组的神经元突起长度较单纯染铅组长 (P <0 0 1) ,使铅浓度为10 - 8~ 10 - 5mol L的神经元生长活力提高 (P <0 0 1)。结论 锂有神经元保护作用 ,而铅对神经元表现出毒性效应 ; Objective To investigate the toxic effects of lead on nervous system and the neuroprotection of lithium, we observed the impact of different dose of lead on the growth and survival of primary cultured cerebrocortical neurons,and the antagonism of lithium to lead. Methods We established the technique of primary culturing cerebrocortical neurons of newborn rats with serum-free medium. We observed the growth and survival of neurons treaded with different dose of lead and 5 mmol/L lithium chloride through microscope, and measured the length of neuritis, we also compared the cell viabilities by MTT reduction assay. Results Lead could limit the growth of neurons, shorten the neuritis, and decrease the neurons viability(P<0.01). Lithium chloride (5mmol/L) had significant protective action on the neurons treated with lead. The length of neuritis were longer than that of the groups treated only with lead(10 -6 mol/L and 10 -5 mmol/L) (P<0.01), and the neurons viability was also higher than that of groups treated with lead (10 -8 -10 -5 mol/L) (P<0.01). Conclusion Lead had the toxic effects on neurons, and lithium could protect the neurons against the toxicity of lead.
出处 《卫生研究》 CAS CSCD 北大核心 2004年第6期671-674,共4页 Journal of Hygiene Research
基金 国家自然科学基金资助项目 (No .39870 689)
关键词 拮抗效应 神经元 神经毒性 lithium, lead, antagonism
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参考文献4

  • 1Manji HK, Moore GJ, Chen G .Lithium at 50: have the neuroprotective effects of this unique cation been overlooked? Biol Psychiatry, 1999,46(7):929-940
  • 2Chen RW,Chuang DM.Long trem lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression.The Journal of Biological Chemistry,1999,274(10):6039-6042
  • 3Hyo JK, Jai SN, Yun SB, et al. Calcium-Dependent Prevention of neuronal apoptosis by lithium ion: essential role of phosphoinositide 3-kinase and phospholipase C. Mol Pharmacol, 2003,64:228-234
  • 4Hashimoto R, Mawchuang LD. Lithium induces brain-derived neurotrophic factor and activates TrkB in rodent cortical neurons:an essential step for neuroprotection against glutamate exitotoxicity. Neuropharmacology,2002,43(7):1173-1179

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