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急性铅应激诱导肝肾损伤及其分子机制初探
引用本文:耿雪侠,戴欣,晁秋杰,杨震,张海军.急性铅应激诱导肝肾损伤及其分子机制初探[J].动物学杂志,2013,48(4):642-649.
作者姓名:耿雪侠  戴欣  晁秋杰  杨震  张海军
作者单位:1. 淮北师范大学生命科学学院 淮北 235000
2. 安徽省涡阳县第三中学 涡阳 233600
基金项目:安徽省教育厅自然科学基金项目(No.KJ2010A299);安徽省高校青年教师资助计划项目(No.2006jql141zd);安徽省自然科学基金项目(No.1208085MC45)
摘    要:利用腹腔注射醋酸铅方法构建了铅染毒小鼠(Mus muscculus)模型,观察了染毒小鼠肝、肾的组织学变化,并通过免疫组织化学方法检测了染毒小鼠肝、肾组织中Caspase-3、Bcl-2和Bax蛋白的表达量.结果发现,急性铅染毒可诱导肝和肾组织学损伤,且在诱导肝细胞和肾细胞凋亡、损伤过程中,随时间的延长,Caspase-3的表达量逐渐增加,而Bcl-2与Bax两蛋白表达量的比值呈逐渐下降趋势,有一定的时效性,染毒48 h后,与对照组相比,均差异极显著,表明铅可能通过影响Caspase-3、Bcl-2和Bax的表达而诱导肝和肾细胞异常凋亡.

关 键 词:铅中毒  细胞凋亡  Caspase-3  Bcl-2  Bax
收稿时间:2012/11/27 0:00:00
修稿时间:2013/5/16 0:00:00

Injury of Liver and Kidney Caused by Acute Lead Poisoning and Related Molecular Mechanisms in Mice
GENG Xue-Xi,DAI Xin,CHAO Qiu-Jie,YANG Zhen and ZHANG Hai-Jun.Injury of Liver and Kidney Caused by Acute Lead Poisoning and Related Molecular Mechanisms in Mice[J].Chinese Journal of Zoology,2013,48(4):642-649.
Authors:GENG Xue-Xi  DAI Xin  CHAO Qiu-Jie  YANG Zhen and ZHANG Hai-Jun
Institution:School of Life Sciences, Huaibei Normal University, Huaibei 235000;School of Life Sciences, Huaibei Normal University, Huaibei 235000;School of Life Sciences, Huaibei Normal University, Huaibei 235000;No.3 High School of Guoyang County, Guoyang 233600, China;School of Life Sciences, Huaibei Normal University, Huaibei 235000
Abstract:Lead-poisoned mouse(Mus muscculus)model was established by intraperitoneal injection of lead acetate. The pathological changes of liver and kidney were examined. The expression alterations of Caspase-3, Bcl-2 and Bax, two apoptosis-related proteins, were also measured. We found that acute lead poisoning caused hepatic and renal injury by inducing cell apoptosis. After lead poisoning, Caspase-3 expression was increased while the ratio of Bcl-2 to Bax decreased in a time-dependent manner. Significant difference in the expression level between control group and experimental group was observed after 48 h of lead exposure. These results suggest that lead poisoning causes hepatic and renal cell apoptosis probably by regulating the expression of Caspase-3, Bcl-2 and Bax.
Keywords:Lead poisoning  Cell apoptosis  Caspase-3  Bcl-2  Bax
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