亚慢性染毒BaP与大鼠海马细胞凋亡及学习记忆损伤的关系
Correlation of Subchronic Exposure to Benzoapyrene with Apoptosis of Hippocampal Neurocytes and Impairment of Learning and Memory in Rats
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摘要:
目的 观察亚慢性染毒苯并a芘(benzoapyrene, BaP)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 BaP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、BaP染毒组0.5、1.5、4.5和 10.0 mg(/kg& #183;bw)。隔日腹腔注射染毒 90 d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、10.0 mg/kg BaP组大鼠平均潜伏期显著高于空白和溶剂对照组和 0.5、1.5 mg/kg BaP组, 差异有统计学意义(P < 0.05); 10.0 mg/kg BaP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、1.5 mg/kg BaP组, 差异有统计学意义 (P < 0.05);4.5 mg/kg BaP 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 mg/kg BaP 组, 差异有统计学意义(P<0.05); 10.0mg/kg BaP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 BaP组, 差异有统计学意义(P < 0.05)。10.0 mg/kg BaP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4.5 mg/kg BaP组, 差异有统计学意义(P < 0.05)。Pearson相关性分析结果显示, BaP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 BaP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 BaP诱发大鼠学习记忆能力损伤的机制之一。 Abstract:Objective To observe the effects of subchronic benzoapyrene (BaP) exposure on cell apoptosis in hippocampus of rats, to analyze its correlation with the impairment of learning and memory, and to explore the mechanism of BaP neurotoxicity. Methods According to the results of Morris water maze test, 48 healthy adult male SD rats were divided into 6 groups:1 blank control, 1 olive control and 4 BaP groups (with 0.5, 1.5, 4.5 and 10.0 mg/kg bw ip injection for 90 days respectively). The learning and memory function was tested by Morris water maze. Cell apoptosis in hippocampus of rats was detected by flow cytometry. Results The Morris water maze test results showed that the 4.5 and 10.0mg/kg BaP groups' average escape latencies were significantly higher than blank control group's, olive control group's, 0.5 and 1.5 mg/kg BaP groups' (P < 0.05). The 10.0 mg/kg BaP group's frequency of crossing platform and swimming time percentage in platform quadrant were significantly lower than blank control group's, olive control group's, and 0.5 and 1.5 mg/kg BaP groups' (P < 0.05). The 4.5 mg/kg BaP group's fr equency of crossing platform and swimming time percentage in platform quadrant were significantly lower than blank control group's, olive control group's, and 0.5 mg/kg BaP group's (P < 0.05). The 10.0 mg/kg BaP group's swimming time in platform quadrant was significantly lower than blank control group's, olive control group's, and 0.5 mg/kg BaP group's (P < 0.05). The 10.0 mg/kg BaP group's early and total hippocampal apoptosis rates were significantly higher than the rest groups'(P < 0.05). Pearson correlation analysis showed that there were positive correlations between early apoptosis rate and average escape latencies (r=0.542, P < 0.05). The early hippocampal apoptosis rate was negatively correlated with and the swimming time in platform quadrant (r=-0.395, P<0.05), and the swimming time percentage in platform quadrant (r=-0.592, P < 0.05). Conclusion Subchronic exposure to BaP leads to cell apoptosis in hippocampus of rats and damage of learning and memory. The results suggest that hippocampal apoptosis in rats may be a possible mechanism to result in learning and memory impairment.
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