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目的探讨N-甲基-D-天门冬氨酸受体(NMDAR)在亚慢性染铝致大鼠学习记忆损害中作用。方法健康成年雄性SD大鼠36只,按体重随机分为对照组、低、中、高剂量麦芽酚铝[Al(mal)3]组(0.41、0.81、1.23 mg/kg),腹腔注射染毒8周后,用Morris水迷宫试验检测大鼠空间学习记忆能力,苏木精-伊红(HE)染色观察大鼠海马组织病理变化,Western-blot方法检测大鼠海马组织NMDAR亚单位NR-2A、NR-2B表达。结果中、高剂量组大鼠找到平台时间分别为(44.12±5.62)、(45.92±13.97)s,均长于对照组的(26.80±1.59)s(P<0.05);中、高剂量染铝组大鼠在目标象限停留时间均明显减少(P<0.05);随着铝剂量增加,大鼠海马锥体层细胞排列分散,细胞数目减少,出现核固缩、空泡变性等病理改变;与对照组NR-2A蛋白表达水平(0.69±0.03)比较,中、高剂量组表达水平[(0.44±0.12)、(0.32±0.19)]均明显降低(P<0.05),且呈剂量效应关系;与对照组比较,各剂量染铝组大鼠NR-2B蛋白水平变化不明显。结论亚慢性染铝可使大鼠学习记忆能力下降,其机制可能与大鼠海马NMDAR亚基蛋白表达改变有关。
Objective To investigate the role of N-methyl-D-aspartate receptor (NMDAR) in learning and memory impairment induced by subchronic aluminum exposure in rats. Methods Thirty - six healthy adult male Sprague - Dawley rats were randomly divided into control group, low, medium and high doses of aluminum maltol [Al (mal) 3] (0.41,0.81,1.23 mg / kg), intraperitoneal injection After 8 weeks, Morris water maze test was used to detect the spatial learning and memory abilities in rats. Hippocampal histopathological changes were observed by hematoxylin-eosin (HE) staining. NMDAR subunit NR-2A , NR-2B expression. Results The plateau time was (44.12 ± 5.62) and (45.92 ± 13.97) s in the medium and high dose groups, both of which were longer than that of the control group (26.80 ± 1.59) s (P <0.05) Rats stayed in the target quadrant for a longer time (P <0.05). With the increase of aluminum dose, the hippocampal pyramidal cells were scattered and the number of cells was decreased. Nuclear condensation and vacuolar degeneration were observed. Compared with the control The expression levels of NR-2A protein in the medium and high dose groups (0.44 ± 0.12, 0.32 ± 0.19) were significantly lower than those in the normal control group (0.69 ± 0.03) (P <0.05) Compared with the control group, the NR-2B protein levels in the aluminum-exposed rats did not change significantly. Conclusion Chronic aluminum exposure can decrease the learning and memory ability of rats, and its mechanism may be related to the change of NMDAR subunit protein expression in the hippocampus of rats.