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目的观察亚慢性染毒偏钒酸钠对大鼠海马细胞凋亡的影响,分析其与学习记忆损伤的关系,探讨偏钒酸钠神经毒性机制。方法选取健康雄性SD大鼠48只,随机分为空白组及低、中、高剂量组。偏钒酸钠饮水染毒3个月后,Morris水迷宫检测大鼠学习记忆能力;流式细胞仪检测海马细胞凋亡。结果中、高染钒组大鼠平均潜伏期显著高于空白组,高钒组高于低钒组,差异有统计学意义(P<0.05);中、高染钒组大鼠穿越平台次数显著低于空白组,差异有统计学意义(P<0.05);中、高染钒组海马细胞早期凋亡率和总凋亡率显著高于空白组,差异有统计学意义(P<0.05)。Spearman相关性分析结果显示,钒染毒大鼠海马细胞早期凋亡率与平均潜伏期呈正相关(rs=0.761,P<0.01),与穿越平台次数呈负相关(rs=-0.502,P<0.01);海马细胞总凋亡率与平均潜伏期呈正相关(rs=0.766,P<0.01),与穿越平台次数呈负相关(rs=-0.487,P<0.01)。结论亚慢性钒中毒可导致大鼠海马细胞凋亡和学习记忆能力损伤,海马细胞凋亡可能是偏钒酸钠诱发大鼠学习记忆能力损伤的机制之一。
Objective To investigate the effect of sub-chronic sodium metavanadate on apoptosis of hippocampal cells in rats and its relationship with learning and memory impairment, and to explore the neurotoxic mechanism of metavanadate sodium. Methods Forty-eight healthy male Sprague-Dawley rats were randomly divided into blank group and low, medium and high dose groups. Sodium metavanadate drinking water for 3 months, Morris water maze test learning and memory ability; flow cytometry detection of hippocampal apoptosis. The results showed that the average latency of rats in high-dye-vanadium group was significantly higher than that in blank group, high-vanadium group was higher than that in low-vanadium group, the difference was statistically significant (P <0.05) In the blank group, the difference was statistically significant (P <0.05). The apoptosis rate and the total apoptosis rate of hippocampal cells in medium and high dye-treated groups were significantly higher than those in blank group (P <0.05). Spearman correlation analysis showed that there was a positive correlation between early apoptotic rate and mean latency of hippocampal cells (r = 0.761, P <0.01) and a negative correlation with the number of crossing platforms (rs = -0.502, P <0.01) ; The total apoptotic rate of hippocampus was positively correlated with the average latency (rs = 0.766, P <0.01), and negatively correlated with the number of crossing platform (rs = -0.487, P <0.01). Conclusion Subchronic vanadium poisoning can induce apoptosis of hippocampal cells and impairment of learning and memory ability. Hippocampal apoptosis may be one of the mechanisms of sodium metavanadate-induced learning and memory impairment in rats.