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[目的]观察亚慢性染毒苯并[a]芘(benzo[a]pyrene,B[a]P)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B[a]P神经毒性机制。[方法]选取健康雄性SD大鼠48只,饲养一周后根据Morris水迷宫检测结果将其分为空白对照组、溶剂对照组、B[a]P染毒组[0.5、1.5、4.5和10.0mg(/kg.bw)]。隔日腹腔注射染毒90d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]4.5、10.0mg/kg B[a]P组大鼠平均潜伏期显著高于空白和溶剂对照组和0.5、1.5mg/kg B[a]P组,差异有统计学意义(P<0.05);10.0mg/kg B[a]P组大鼠穿越平台次数和平台象限滞留时间百分比显著低于空白和溶剂对照组及0.5、1.5mg/kg B[a]P组,差异有统计学意义(P<0.05);4.5mg/kg B[a]P组大鼠穿越平台次数和平台象限滞留时间百分比显著低于空白和溶剂对照组及0.5mg/kg B[a]P组,差异有统计学意义(P<0.05);10.0mg/kg B[a]P组大鼠平台象限滞留时间显著低于空白和溶剂对照组及0.5mg/kg B[a]P组,差异有统计学意义(P<0.05)。10.0mg/kg B[a]P组海马细胞早期凋亡率和总凋亡率显著高于空白和溶剂对照组及0.5、1.5和4.5mg/kg B[a]P组,差异有统计学意义(P<0.05)。Pearson相关性分析结果显示,B[a]P染毒大鼠海马细胞早期凋亡率与平均潜伏期呈正相关(r=0.542,P<0.05);海马细胞早期凋亡率与平台象限滞留时间呈负相关(r=-0.395,P<0.05)、与平台象限滞留时间百分比呈负相关(r=-0.592,P<0.05)。[结论]亚慢性染毒B[a]P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B[a]P诱发大鼠学习记忆能力损伤的机制之一。
[Objective] To observe the effect of subchronic benzo [a] pyrene (B [a] P) on the apoptosis of hippocampal cells in rats and its relationship with learning and memory impairment, ] P neurotoxic mechanism. [Method] Forty-eight healthy male Sprague-Dawley rats were selected for one week and divided into blank control group, solvent control group, B [a] P group [0.5, 1.5, 4.5 and 10.0 mg (/kg.bw)]. The rats were injected intraperitoneally every other day for 90 days. Morris water maze was used to detect the learning and memory ability of rats. The apoptosis of hippocampal cells was detected by flow cytometry. [Results] The average latency of rats in 4.5 and 10.0 mg / kg B [a] P group was significantly higher than that of blank and solvent control groups and 0.5 and 1.5 mg / kg B [a] P groups (P <0.05 ); The percentage of rats in the 10.0 mg / kg B [a] P group crossing the platform and the platform quadrant retention time were significantly lower than those in the blank and solvent control groups and 0.5 and 1.5 mg / kg B [a] P groups (P <0.05). The percentage of transit time in plateau and quadrant in 4.5 mg / kg B [a] P group was significantly lower than that in blank and solvent control group and 0.5 mg / kg B [a] P group (P <0.05). The retention time in the platform quadrant of the 10.0 mg / kg B [a] P group was significantly lower than that of the blank control group and the solvent control group and 0.5 mg / kg B [a] P group P <0.05). The early apoptosis rate and the total apoptosis rate of hippocampal cells in 10.0 mg / kg B [a] P group were significantly higher than those in blank and solvent control groups and 0.5, 1.5 and 4.5 mg / kg B [a] P groups (P <0.05). Pearson correlation analysis showed that the apoptotic rate of hippocampal cells in B [a] P-exposed rats was positively correlated with the mean latency (r = 0.542, P <0.05); the early apoptotic rate of hippocampal cells was negative (R = -0.395, P <0.05), and negatively correlated with the percentage of residence time in the platform quadrant (r = -0.592, P <0.05). [Conclusion] Subchronic exposure to B [a] P can induce the apoptosis of hippocampal cells and the impairment of learning and memory ability. The apoptosis of hippocampus may be one of the mechanisms of B [a] P induced learning and memory impairment in rats.