慢性铝暴露对大鼠脑皮质与外周血淋巴细胞NMDAR1的影响

发布时间：2018-05-04 18:40

本文选题：铝暴露 + 脑皮质　；参考：《卫生研究》2017年01期

【摘要】：目的研究慢性铝暴露对脑皮质与外周血淋巴细胞N-甲基-D-天冬氨酸受体1(NMDAR1)的影响,探讨外周血淋巴细胞NMDAR1作为外周血中铝暴露生物标志物的可能性。方法选取2月龄健康雄性清洁级SD大鼠32只,按体重随机分为空白组和铝低、中、高剂量组,空白组饮用自来水,铝低、中、高剂量组分别给予20、120、720 mg/L Al Cl3饮水,大鼠每日饮水约10 m L/100 g,连续染毒360 d。染毒结束,采用石墨炉原子吸收法测定血浆铝和脑铝含量,采用实时荧光定量聚合酶链反应法(RT-PCR)测定脑皮质与外周血淋巴细胞中NMDAR1基因相对表达量,酶联免疫吸附法(ELISA)测定脑皮质和外周血淋巴细胞中NMDAR1蛋白含量。结果对照组及铝低、中、高剂量组血浆铝含量分别为69.88、83.10、87.06和134.60μg/L,铝低、中、高剂量组高于对照组,差异有统计学意义(P0.05);脑铝含量分别为0.065、0.102、0.139和0.228μg/mg,铝低、中、高剂量组高于对照组,差异有统计学意义(P0.05)。NMDAR1基因表达随铝剂量升高呈下降趋势,脑皮质基因相对表达量铝中、高剂量组低于对照组(P0.05);外周血淋巴细胞NMDAR1基因表达铝中、高剂量组低于铝低剂量组和对照组(P0.05),铝中、高剂量组之间比较差异无统计学意义(P=0.167)。脑皮质NMDAR1蛋白含量铝高剂量组低于对照组、铝低剂量组(P0.05);铝中剂量组低于对照组(P0.05);淋巴细胞NMDAR1蛋白含量铝高剂量组低于对照组、铝低剂量组(P0.05),与铝中剂量组比较差异无统计学意义(P=0.159)。结论慢性铝暴露可影响大鼠脑皮质与外周血淋巴细胞NMDAR1基因相对表达量和蛋白表达,随铝剂量的增加基因相对表达量和蛋白表达下降,可将NMDAR1作为铝暴露外周生物标志物进一步研究。
[Abstract]:Objective to study the effect of chronic aluminum exposure on N- methyl -D- aspartic acid receptor 1 (NMDAR1) in the cerebral cortex and peripheral blood lymphocytes and to explore the possibility of NMDAR1 as a biomarker in the peripheral blood of the peripheral blood. Methods 32 healthy male SD rats were selected and divided into blank group and low aluminum by weight randomly. High dose group, blank group drinking tap water, aluminum low, middle, high dose group were given 20120720 mg/L Al Cl3 drinking water respectively, rats drinking water about 10 m L/100 g daily, continuous exposure to 360 D. poisoning end, graphite furnace atomic absorption method was used to determine plasma aluminum and brain aluminum content, real-time fluorescence quantitative polymerase chain reaction (RT-PCR) was used for the determination of cerebral cortex and cerebral cortex. The relative expression of NMDAR1 gene in peripheral blood lymphocytes and the content of NMDAR1 protein in cerebral cortex and peripheral blood lymphocytes were measured by enzyme linked immunosorbent assay (ELISA). Results of the control group and aluminum low, middle, high dose group, the plasma aluminum content was 69.88,83.10,87.06 and 134.60 mu g/L respectively, and the high dose group was higher than the control group, the difference was statistically significant. The content of Al (P0.05) was 0.065,0.102,0.139 and 0.228 g/mg respectively, and the high dose group of aluminum was higher than that of the control group. The difference was statistically significant (P0.05), the expression of.NMDAR1 gene decreased with the increase of aluminum dose, and the relative expression of aluminum in the cerebral cortex was lower than that of the control group (P0.05), and the NMDAR1 gene expression in peripheral blood lymphocytes was expressed. In aluminum, the high dose group was lower than the low dose al Group and the control group (P0.05), and there was no significant difference between the aluminum and the high dose groups (P=0.167). The high dose group of NMDAR1 protein in the cerebral cortex was lower than the control group, the low dose al Group (P0.05), the middle dose of aluminum group was lower than the control group (P0.05), and the high dose group of lymphocyte NMDAR1 protein content was lower than that of the high dose group. There was no significant difference between the low dose al Group (P0.05) and the aluminum dose group (P=0.159). Conclusion chronic aluminum exposure could affect the relative expression and protein expression of NMDAR1 gene in the cerebral cortex and peripheral blood lymphocytes of rats. The relative expression of gene and the expression of protein decreased with the increase of aluminum dose, and NMDAR1 could be used as the aluminum exposure week. Further study of biomarkers.

【作者单位】：山西医科大学公共卫生学院劳动卫生教研室;
【基金】：国家自然科学基金重点项目(No.81430078) 山西省教育厅研究生教育创新项目(No.2016SY029)
【分类号】：R114

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