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目的观察偏钒酸钠亚慢性经口染毒所致大鼠学习记忆损伤情况,探讨其对纹状体神经细胞凋亡的影响。方法无特定病原体级健康雄性SD大鼠32只,随机分为对照组及低、中、高剂量组,每组8只。分别予质量浓度为0.0、0.5、1.0、2.0 g/L偏钒酸钠水溶液经口饮水染毒3个月后,采用Morris水迷宫实验测试大鼠学习记忆能力,分离大鼠纹状体观察神经细胞形态学改变并以流式细胞仪检测其神经细胞凋亡率。结果对照组和低、中、高剂量组大鼠平均逃避潜伏期分别为(37.43±8.82)、(45.71±12.44)、(59.74±22.91)、(68.45±12.06)s;中剂量组大鼠逃避潜伏期高于对照组(P<0.05),高剂量组大鼠逃避潜伏期分别高于对照组和低剂量组(P<0.05)。4组大鼠穿越平台次数中位数(M)分别为3.5、3.0、2.0和2.0次;中和高剂量组穿越平台次数均低于对照组(P<0.05)。4组大鼠脑纹状体神经细胞早期凋亡率M分别为2.15%、5.45%、9.50%和13.55%,晚期凋亡率M分别为0.05%、0.15%、0.35%和0.75%,总凋亡率M分别为2.35%、5.60%、9.80%和14.65%;中和高剂量组纹状体神经细胞早期凋亡率、总凋亡率均分别高于对照组(P<0.05)。病理组织学检查结果显示:大鼠纹状体组织疏松、水肿、空泡变性,可见细胞凋亡形态。Spearman相关分析显示:钒染毒大鼠的逃避潜伏期与纹状体神经细胞早期凋亡率和总凋亡率均呈正相关[Spearman相关系数(rS)分别为0.615和0.565,P<0.05];穿越平台次数与纹状体神经细胞早期凋亡率和总凋亡率均呈负相关(rS分别为-0.450和-0.483,P<0.05)。结论偏钒酸钠可通过介导纹状体神经细胞凋亡增加而损伤大鼠学习记忆能力。
Objective To observe the learning and memory impairment induced by sub-chronic oral administration of sodium metavanadate in rats and to explore its effect on neuronal apoptosis in the striatum. Methods Thirty-two healthy male SD rats without specific pathogen were randomly divided into control group and low, medium and high dose groups, with 8 in each group. After being exposed to orally drinking water for three months at concentrations of 0.0, 0.5, 1.0 and 2.0 g / L sodium metavanadate respectively, Morris water maze test was used to study the learning and memory abilities in rats. Morphological changes were observed by flow cytometry and apoptosis rate of neurons. Results The mean escape latency of the control group and the low, medium and high dose groups were (37.43 ± 8.82), (45.71 ± 12.44) and (59.74 ± 22.91) and (68.45 ± 12.06) s, respectively. The mean escape latency (P <0.05). The escape latency of high dose group was higher than that of control group and low dose group (P <0.05). The median number (M) of traversing platforms of the four groups of rats was 3.5, 3.0, 2.0 and 2.0 times, respectively. The number of passing through the platform in the medium and high dose groups was lower than that of the control group (P <0.05). The early apoptotic rate of brain striatum in the 4 groups was 2.15%, 5.45%, 9.50% and 13.55% respectively. The rates of late apoptosis were 0.05%, 0.15%, 0.35% and 0.75% The rates of M and M were 2.35%, 5.60%, 9.80% and 14.65%, respectively. The rates of early apoptosis and total apoptosis in the medium and high dose groups of striatum were higher than those of the control group (P <0.05). Histopathological examination showed that: the rat striatum tissue loose, edema, vacuolar degeneration, visible apoptotic morphology. Spearman correlation analysis showed that the escape latency of vanadium-exposed rats was positively correlated with the early apoptosis rate and total apoptosis rate of striatal neurons [Spearman’s correlation coefficient (rS) was 0.615 and 0.565 respectively, P <0.05] There was a negative correlation between the number of plateau and the early apoptosis rate and the total apoptosis rate of striatal neurons (rS = -0.450 and -0.483, respectively, P <0.05). Conclusion Sodium metavanadate can impair learning and memory in rats by mediating the increase of neuron apoptosis.