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目的探讨燃煤型氟中毒大鼠智力变化及其发生机制。方法复制燃煤型氟中毒大鼠模型,用Morris水迷宫检测大鼠行为学改变;蛋白印迹及实时荧光定量PCR检测信号转导系统细胞外调节蛋白激酶1/2(ERK1/2)表达水平。结果高、低氟组大鼠逃避潜伏时间分别为(14.44±10.18)和(11.64±7.08)s,较对照组明显延长(P<0.05);氟中毒大鼠第7 d穿台次数及逗留平台相限时间均较对照组减少(P<0.05);染氟组大鼠脑组织中ERK1/2磷酸化蛋白较对照组升高1.5~2.3倍(P<0.05),mRNA表达水平较对照组升高2.0~3.5倍(P<0.05),呈剂量-效应关系。结论燃煤型氟中毒可引起大鼠学习、记忆能力降低,其机制可能与脑组织中ERK/MAPK信号转导通路的激活有关。
Objective To investigate the changes of intelligence in rats with fluorosis and its mechanism. Methods The model of fluorosis in coal-fueled rats was duplicated. Morris water maze was used to detect the behavioral changes. Western blotting and real-time fluorescence quantitative PCR were used to detect the expression of extracellular regulated protein kinase 1/2 (ERK1 / 2) in the signal transduction system. Results The escape latency of rats in high and low fluoride groups were (14.44 ± 10.18) and (11.64 ± 7.08) s respectively, significantly longer than those in control group (P <0.05) (P <0.05). Compared with the control group, ERK1 / 2 phosphorylated protein increased by 1.5- to 2.3-fold (P <0.05) and the mRNA expression of ERK1 / 2 increased High 2.0 to 3.5 times (P <0.05), a dose-response relationship. Conclusion Burning fluorosis can cause learning and memory impairment in rats, and its mechanism may be related to the activation of ERK / MAPK signal transduction pathway in brain tissue.