急性铅应激诱导肝肾损伤及其分子机制初探
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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)


Injury of Liver and Kidney Caused by Acute Lead Poisoning and Related Molecular Mechanisms in Mice
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    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。

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    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.

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耿雪侠,戴欣,晁秋杰,杨震,张海军.2013.急性铅应激诱导肝肾损伤及其分子机制初探.动物学杂志,48(4):642-649.

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  • 收稿日期:2012-11-27
  • 最后修改日期:2013-05-16
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  • 在线发布日期: 2013-08-21
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