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作 者:莫颂轶[1] 张丽凤 黄彦峰[1] 余双全 廖素婵 黄永毅[1] 梁祚仁[1] 黎昀[1] 蒋敏丽[1] 黄俊杰[1] MO Songyi;ZHANG Lifeng;HUANG Yanfeng;YU Shuangquan;LIAO Suchan;HUANG Yongyi;LIANG Zuoren;LI Yun;JIANG Minli;HUANG Junjie
机构地区:[1]右江民族医学院应用生理研究室,广西百色533000
出 处:《中国比较医学杂志》2018年第7期63-67,共5页Chinese Journal of Comparative Medicine
基 金:广西壮族自治区教育厅高校科研重点项目(编号:ZD2014101)
摘 要:目的通过观察慢性铝中毒小鼠学习记忆能力的变化以及大脑皮层乙酰胆碱(ACh)、β-内啡肽(β-EP)、超氧化物歧化酶(SOD)和丙二醛(MDA)含量的变化,探讨铝中毒导致小鼠认知能力障碍的机制。方法用Al Cl3水溶液拌入饲料中喂养小鼠,建立不同程度铝中毒模型小鼠。染毒三个月后,Y型迷宫实验测试小鼠学习记忆能力,测定大脑皮层ACh、β-EP、SOD和MDA含量。结果与对照组相比,中剂量、高剂量铝中毒组小鼠学习测试次数和记忆错误次数均明显增多,大脑皮层ACh、β-EP和SOD含量均明显降低,而大脑皮层MDA含量却升高。中剂量、高剂量铝中毒组小鼠大脑皮层中ACh、β-EP和SOD均与相应同剂量组学习测试次数和记忆错误次数均呈负相关;高剂量铝中毒组MDA含量与同剂量组学习测试次数和记忆错误次数均呈正相关。结论铝可能通过降低大脑皮层中ACh、β-EP和SOD含量,提高MDA含量,进而影响小鼠学习与记忆能力,这可能是铝中毒致小鼠认知能力障碍的机制之一。Objective To investigate the mechanisms underlying cognitive impairment induced by chronic aluminum exposure through observing the relationships between learning and memory functions and levels of ACh,β-EP,SOD,and MDA in the mouse cerebral cortex.Methods Mice were fed diets containing various doses of AlCl 3.Their learning and memory abilities were measured by the Y maze test,and levels of ACh,β-EP,SOD,and MDA in the mouse cerebral cortex were measured at end of the experiment.Results The learning times and memory errors in groups administered moderate and high doses of aluminum were significantly increased compared with those in the control group.The levels of ACh,β-EP,and SOD in the cerebral cortex were decreased significantly,whereas the MDA level in the cerebral cortex was increased in groups administered moderate and high doses of aluminum compared with the control group.ACh,β-EP and SOD levels in the cerebral cortex were negatively correlated with learning times and memory errors in mice administered moderate and high doses of aluminum.MDA levels were positively correlated with learning times and memory errors in mice administered the high dose of aluminum.Conclusions Aluminum reduces the abilities of learning and memory in mice,possibly through decreasing the levels of ACh,β-EP,and SOD,and increasing the MDA level in the cerebral cortex,which may be the mechanisms underlying aluminum-induced cognitive impairment in mice.
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