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作 者:王福俤[1] 赵法伋[1] 郭俊生[1] 景乃禾[2]
机构地区:[1]第二军医大学军队卫生学教研室,上海200433 [2]中国科学院上海生物化学研究所,上海20003
出 处:《卫生研究》2000年第3期156-158,共3页Journal of Hygiene Research
基 金:国家自然科学基金!( No.3 9770 64 3 ;3 9970 64 1);全军"九五"青年基金!( No.98Q0 43
摘 要:为探讨发育期锌缺乏降低脑组织微管聚合作用的可能机理 ,作者观察了孕期及哺乳期锌缺乏母鼠其仔代成年时的学习能力以及脑组织α微管蛋白 (α- Tub)、β-微管蛋白 (β- Tub)和微管相关蛋白 2 (MAP2 )表达水平。给处于孕期及哺乳期 ICR母鼠喂饲含不同锌水平的实验饲料 ,饲料锌水平分别为 1、5、30及 10 0 mg/kg。在穿梭箱内检测实验仔鼠成年 (70日龄 )时的学习能力 ,然后采用 Western blot技术检测其脑组织中 α-Tub、β- Tub及 MAP2的表达情况。行为学检测发现缺锌组 (1和 5 mg/ kg)达到学会标准所需次数明显多于非缺锌组 (30及 10 0 m g/ kg) ,表明缺锌小鼠学习能力受损 ;比较各实验组 α- Tub、β- Tub及 MAP2表达量发现 ,缺锌组α- Tub、β- Tub及 MAP2杂交信号明显弱于非缺锌组。蛋白表达量顺序均为 1m g/ kg组 <5 mg/ kg组 <30 mg/ kg组 <10 0 mg/ kg组 ,表明 α- Tub、β- Tub及 MAP2的表达水平与膳食锌呈正依赖关系。α- Tub、β-Tub及 MAP2表达量降低可能是脑组织微管聚合作用下降的重要机制所在 ,并且与锌缺乏引发的脑功能损伤密切相关。To probe into the mechanism of zinc deficiency on microtubule polymerization impairment, the learning ability and the levels of α tubulin,β tubulin and microtubule\|associated protein 2 expression in the brain of zinc deficient offsprings, maternal ICR mice were fed with experiment diets containing different levels of zinc(1,5,30 and 100mg/kg) during pregnancy and lactation respectively.On the postnatal day 70 of offsprings, the learning ability and the expression of α tubulin,β tubulin and microtubule\|associated protein 2 in the brain were examined by shuttle box and Western blot assays respectively. The results showed that the number of trials needed to reach the learning criterion for zinc deficient groups (1 and 5mg/kg)was much higher than that for non zinc deficient groups (30 and 100mg/kg).The levels of α tubulin,β tubulin and microtubule\|associated protein 2 expression in the brain of zinc deficient offsprings (1 and 5mg/kg) were lower than those in the brain of offsprings whose dams fed with zinc adequatedly supplied diet (30mg/kg) and zinc supplemented supplied diet (100mg/kg) respectively. These results suggested that the inhibition of α tubulin,β tubulin and microtubule\|associated protein 2 expression might be the most important mechanism of microtubule polymerization decline resulting from zinc deficiency, which had close relationship with brain function impairment.
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