论文部分内容阅读
目的探讨铅和高脂饮食联合暴露对大鼠学习记忆功能损伤及海马组织炎症因子的影响。方法无特定病原体级成年雄性SD大鼠随机分为对照组、高脂饮食组、铅暴露组和联合暴露组,每组10只。对照组大鼠予基础饲料喂养,高脂饮食组大鼠予高脂饲料喂养,铅暴露组大鼠予基础饲料喂养同时饮用质量浓度为400 mg/L的醋酸铅饮用水;联合暴露组大鼠予高脂饲料喂养同时饮用质量浓度为400 mg/L的醋酸铅饮用水。隔周测量大鼠体质量。暴露9周后,采用Morris水迷宫实验检测大鼠的学习记忆能力,采用酶标仪检测血清中总胆固醇、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL)、高密度脂蛋白胆固醇(HDL)的水平,采用电感耦合等离子体-质谱仪检测海马组织中铅水平,采用酶联免疫吸附实验检测海马组织中肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-1β、IL-4、IL-6和干扰素-γ(IFN-γ)的水平。结果自第3周起,高脂饮食组与联合暴露组大鼠的体质量均高于对照组(P<0.05),联合暴露组体质量高于铅暴露组(P<0.05)。与对照组比较,高脂饮食组、铅暴露组及联合暴露组大鼠逃避潜伏期均延长(P<0.05),穿越平台次数均下降(P<0.05);联合暴露组大鼠逃避潜伏期分别较高脂饮食组及铅暴露组延长(P<0.05)。分别与对照组和铅暴露组比较,高脂饮食组和联合暴露组大鼠血清TG和LDL水平均升高(P<0.05),HDL水平均降低(P<0.05)。分别与对照组和高脂饮食组比较,铅暴露组和联合暴露组大鼠海马组织中铅水平均升高(P<0.05)。与对照组比较,其余3组大鼠海马组织中TNF-α、IL-6、IL-1β、IFN-γ水平均升高(P<0.05),铅暴露组和联合暴露组大鼠海马组织中IL-4水平均升高(P<0.05)。联合暴露组大鼠海马组织中IL-1β水平分别高于高脂饮食组和铅暴露组(P<0.05)。结论铅和高脂饮食联合暴露对大鼠学习记忆能力的下降产生协同效应;IL-1β可能参与了铅和高脂饮食联合暴露所致神经损伤协同作用的过程。
Objective To investigate the effects of lead and high-fat diet combined with learning and memory impairment and hippocampal inflammatory cytokines in rats. Methods Adult male SD rats without specific pathogen were randomly divided into control group, high fat diet group, lead exposure group and combined exposure group, with 10 rats in each group. The rats in the control group were fed with basal diet, the rats in the high-fat diet group were fed with high-fat diet, the rats in the lead-exposed group were fed with the basic diet and the drinking water with the concentration of 400 mg / L of lead acetate. The rats in the combined exposure group High-fat diets were fed with lead acetate drinking water at a concentration of 400 mg / L. Body mass was measured every other week. After 9 weeks of exposure, Morris water maze test was used to detect the learning and memory abilities of rats. Serum levels of total cholesterol, triglyceride (TG), low density lipoprotein cholesterol (LDL) and high density lipoprotein cholesterol (HDL). The level of lead in hippocampus was detected by inductively coupled plasma mass spectrometry. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL- IL-4, IL-6 and interferon-γ (IFN-γ) levels. Results From the third week onwards, the body weight of rats in the high-fat diet group and the combined exposure group was higher than that of the control group (P <0.05). The body weight of the combined exposure group was higher than that of the lead exposure group (P <0.05). Compared with the control group, the escape latency of rats in the high-fat diet group, the lead exposure group and the combined exposure group were prolonged (P <0.05), and the number of crossing the platform decreased (P <0.05); the escape latency of the rats in the combined exposure group was higher Fat diet group and lead exposure group prolonged (P <0.05). Compared with the control group and the lead exposure group, the levels of serum TG and LDL in the high-fat diet group and the combined exposure group were both increased (P <0.05), and the HDL levels were decreased (P <0.05). Compared with the control group and the high-fat diet group respectively, the levels of lead in the hippocampus of the lead exposure group and the combined exposure group were increased (P <0.05). Compared with the control group, the levels of TNF-α, IL-6, IL-1β and IFN-γ in the hippocampus were significantly increased in the other three groups (P <0.05) IL-4 levels were increased (P <0.05). The levels of IL-1β in the hippocampus of the combined exposure group were higher than those in the high-fat diet group and the lead exposure group respectively (P <0.05). Conclusion The combined exposure of lead and high-fat diet has a synergistic effect on the decline of learning and memory in rats. IL-1β may be involved in the synergistic effect of nerve injury induced by exposure to lead and high-fat diet.