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机构地区:[1]中国医科大学基础医学院生物化学与分子生物学教研室,辽宁沈阳110001
出 处:《毒理学杂志》2007年第5期387-388,共2页Journal of Toxicology
基 金:国家自然科学基金项目(30371229)
摘 要:目的通过进一步研究慢性铝暴露引起大鼠海马细胞内[Ca2+]i和钙调蛋白激酶激酶Ⅱ(CaMⅡ)蛋白表达的变化,来探讨铝损害学习记忆的作用机制。方法选择断乳后Wistar大鼠,以含有不同浓度AlCl3的水进行饲养。3个月后,取海马测定细胞内[Ca2+]i,用Western blotting方法检测CaMKⅡ的蛋白表达。结果(1)各染铝组的[Ca2+]i与对照组比较明显降低,差异有统计学意义(P<0.01),但各染铝组间差异无统计学意义;(2)各染铝组CaMKⅡ蛋白表达与对照组比较也显著降低,并成剂量关系,差异有统计学意义(P<0.01)。结论铝能够降低大鼠海马细胞内的[Ca2+]i浓度并造成CaMKⅡ的蛋白表达降低,从而损伤学习记忆功能。Objective To go deep into the mechanism for chronic aluminum-induced impairments to learning and memory by studying the change of [ Ca^2+ ]i and concentration of calcium ( [ Ca^2+ ]i ) calciurrdcalmodulin-dependent kinase Ⅱ ( CaMK Ⅱ ). Methods The ablactated Wistar rats were used to establish the chrenic-aluminium exposed models by the garages of aluminum chloride ( AlCl3 ) of different concentrations in the drinking water and measured the [ Ca^2+ ]i in hippocampi of the rats. Western Blot was used to determine CaMK II contents in hippocampi. Results (1) [ Ca^2+ ]i in AlCl3 exposed groups was obviously lower than that in control group ( P 〈 0.01 ) but there was no significant difference among aluminum treated groups. (2)The content of CaMK II in hippocampus of AlCl3-exposed groups fell down in a dose-dependent manner comparing with that of control group ( P 〈 0.01 ). Conclusion Chronic aluminum exposure can affect [ Ca^2+ ]i and CaMKⅡ content, which play most important roles in learning and memory, and impair the ability of learning and memory.
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