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机构地区:[1]贵州电力职工医院病理科,贵州贵阳550002 [2]贵阳医学院病理学及分子生物学教研室,贵州贵阳550004
出 处:《贵州医药》2013年第1期8-11,共4页Guizhou Medical Journal
基 金:国家自然科学基金资助项目(81160335);科技部国际合作项目(2010DFB30530)
摘 要:目的复制燃煤污染型氟中毒大鼠模型,检测其细胞外信号调节激酶/90ku核小体S6激酶(ERK/p-90RSK)信号通路的变化,探讨燃煤污染型氟中毒中枢神经系统损害的发病机制。方法以贵州省地方性燃煤污染型氟中毒重病区燃煤烘烤的玉米为主要饲料,复制不同摄氟剂量的慢性氟中毒大鼠模型,实验期为6个月。Western-blotting法检测ERK/p-90RSK信号通路相关磷酸化蛋白的表达水平。结果成功建造燃煤污染型氟中毒大鼠模型。检测结果显示,染氟组中大鼠脑组织中p-ERK1/2和p-90RSK蛋白的表达均高于对照组,且高剂量染氟组高于低剂量染氟组,差异有统计学意义(P<0.05)。结论燃煤污染型氟中毒可引起大鼠脑组织中ERK信号转导通路的过度激活,而p-90RSK的激活可能是氟中毒大鼠的反馈性保护机制。Objective To discuss the mechanism of central nervous system damage in coal-buring fluorosis and the fluoride pollution rat models were created to detect change of ERK /P90RSK signal transduction pathway. Methods The fluoride pollution models were created by feeding rats with coalburning pollution corn for 6 moths. Phosphorylated protein of ERK /P90RSK signal transduction pathway was measured by Western-blot method, Resullts Coal-buring fluorosis rat models were estab-lished. Western blot showed the expression of p-ERK1/2 and p-90RSK was improved with the concentration of fluorine(P〈0.05). Conclusion ERK signal transduction pathway was activated in coal-buring fluorosis rat models. The activation of p-90RSK may result in the feedback protection of coal-buring fluorosis rat models.
关 键 词:氟中毒 大鼠 脑组织 细胞外信号调节激酶 90ku核小体S6激酶
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