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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 investigate the possible mechanism of zinc deficiency during development in reducing microtubule polymerization in brain tissue, the authors observed the learning ability of adult Zinc-deficient males during adulthood during pregnancy and lactation, and the effects of α-tubulin, β - Tubulin (tubulin) and microtubule-associated protein 2 (MAP2) expression levels. ICR female rats fed during pregnancy and lactation were fed experimental diets containing different levels of zinc with feed zinc levels of 1, 5, 30 and 100 mg / kg, respectively. The learning ability of adult offspring of experimental pups (70 days old) was detected in the shuttle box, and the expression of α-Tub, β-Tub and MAP2 in brain tissue were detected by Western blot. Behavioral testing found that zinc deficiency (1 and 5 mg / kg) required significantly more learners to reach the standard than non-zinc deficient groups (30 and 100 mg / kg), indicating impaired learning ability in zinc-deficient mice; The expression of α-Tub, β-Tub and MAP2 in the experimental group was found that the signal of α-Tub, β-Tub and MAP2 in the zinc-deficient group was significantly weaker than that of the non-zinc-deficient group. Protein expression levels were 1m g / kg group <5 mg / kg group <30 mg / kg group <10 0 mg / kg group, indicating that α-Tub, β- Tub and MAP2 expression was positively correlated with dietary zinc . The decrease of α-Tub, β-Tub and MAP2 may play an important role in the decrease of microtubule polymerization in brain tissue, and is closely related to the impairment of brain function induced by zinc deficiency.