亚慢性砷中毒对大鼠肝脏自噬的抑制作用  

The Inhibitory Effect of Autophagy in Liver Induced by Chronic Arsenic Exposure

作　　者：张建彬[1] 净锦飞[1] 蔡同建[1] 骆文静[1] 赵芳[1] 姚婷[1] 沈学锋[1] 杜可军[1] 陈耀明[1] 李丹[1] 郑刚[1] 陈景元[1] 

机构地区：[1]第四军医大学劳动与环境卫生学教研室,陕西西安710032

出　　处：《现代生物医学进展》2010年第21期4045-4048,共4页Progress in Modern Biomedicine

基　　金：国家自然科学基金面上项目(30800898)

摘　　要：目的:在建立亚慢性砷暴露模型的基础上,探讨砷暴露对SD大鼠肝脏自噬水平的影响。方法:出生21天断乳雄性SD大鼠分为不同水平砷暴露组,通过饮水给与NaAsO2的方式染毒;全自动生化分析仪检测血清肝功能项目的变化;HE染色检测肝脏组织病理学改变;透射电镜法超微结构的改变。Western blot方法检测自噬相关蛋白Beclin1、LC3表达水平变化。结果:砷暴露组肝脏出现显著的异常,同时伴随肝组织形态学改变。于是此同时,LC3Ⅱ/LC3Ⅰ比值以及beclin1的表达水平均随着砷作用浓度的升高而降低。结论:亚慢性砷暴露在诱导肝脏损伤的同时可伴随自噬水平的抑制,这种水平的改变可能参与了砷的肝脏毒性。Objective：To investigate the effect of arsenic exposure on the autophagy in rat liver by establishing chronic arsenic-ex-posure model.Methods：The 21 days after birth in male SD rats were treated by different doses of arsenic which was carried out water containing NaAsO2.An automatic automatic biochemistry analyzer was used to determine the indexes for hepatic function;HE staining was used to determine the histopathological changes;transmission electron microscope was used to determine the ultrastructural changes;and Western blot was used to determine the expression of autophagy-related proteins including Beclin1 and LC3.Results：The exposure to arsenic resulted significant disfunction of liver,together with special histomorphology changes.Furthermore,the increased arsenic concentration resulted in the decrease of LC3Ⅱ/LC3Ⅰand Beclin 1 level.Conclusion：The exposure to arsenic may lead to the damage of liver and the inhibition of autophagy,which may play a role in arsenic-induced liver toxicity.

关 键 词：砷 肝脏 自噬 

分 类 号：Q95-3[生物学—动物学] R595[医药卫生—内科学]