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作 者:张玲[1] Hossmann Alex
机构地区:[1]东南大学附属中大医院神经内科,江苏南京210009 [2]Max-planck Institute for Neurology
出 处:《现代医学》2007年第2期105-108,共4页Modern Medical Journal
摘 要:目的对L1细胞黏附分子(L1 cell adhesion molecule,L1CAM)基因敲除(gene knockout,KO)小鼠的各脑区脑局部血流量、ATP含量和蛋白合成率进行分析,探讨L1CAM基因缺失对小鼠脑局部代谢功能有无影响。方法用放射性自显影方法测定L1 KO小鼠和野生型对照组小鼠大脑局部血流量和蛋白质合成率,用生物荧光影像技术测定两组ATP含量,并将两组数据进行比较。结果与野生型小鼠相比,L1 KO小鼠局部脑血流量、ATP含量和蛋白质合成率差异均无统计学意义(均P>0.05)。结论L1CAM基因缺失对小鼠脑局部代谢功能无明显影响,提示L1 KO小鼠可作为研究L1CAM在脑缺血中作用的动物模型。Objective To analyze focal cerebral blood flow, ATP content and protein synthesis of L1 knockout ( L1 KO) mice and to evaluate if lack of L1 gene will have some influence on mice brain metabolism. Methods Metabolic functions were studied by [ 14^C ] antipyrine autoradiography for the measurement of cerebral blood flow (CBF), by 3H-leucine autoradiography for the measurement of cerebral protein synthesis (CPS) and by regional ATP bioluminescent imaging for the measurement of ATP content. Results Compared with wild type mice, there was no significant difference in CBF, CPS and ATP levels in L1 KO mice ( P 〉 0.05 ). Conclusion Without obvious influence in brain metabolic functions, L1 KO mice is an useful animal model for investigation of the role of L1 in brain ischemia.
分 类 号:R743.3[医药卫生—神经病学与精神病学] R-332[医药卫生—临床医学]
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