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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.
急性铅应激诱导肝肾损伤及其分子机制初探
Injury of Liver and Kidney Caused by Acute Lead Poisoning and Related Molecular Mechanisms in Mice
投稿时间:2012-11-27  修订日期:2013-05-16
DOI:
中文关键词:  铅中毒  细胞凋亡  Caspase-3  Bcl-2  Bax
英文关键词:Lead poisoning  Cell apoptosis  Caspase-3  Bcl-2  Bax
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)
作者单位
耿雪侠 淮北师范大学生命科学学院 淮北 235000 
戴欣 淮北师范大学生命科学学院 淮北 235000 
晁秋杰 淮北师范大学生命科学学院 淮北 235000 
杨震 安徽省涡阳县第三中学 涡阳 233600 
张海军 淮北师范大学生命科学学院 淮北 235000 
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中文摘要:
      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。
英文摘要:
      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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