• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Alcohol >Increased DNA double-strand break was associated with downregulation of repair and upregulation of apoptotic factors in rat hippocampus after alcohol exposure
【24h】

Increased DNA double-strand break was associated with downregulation of repair and upregulation of apoptotic factors in rat hippocampus after alcohol exposure

机译：增加DNA双链断裂与酒精暴露后大鼠海马凋亡因子的修复和上调的下调有关

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Binge drinking is known to cause damage in critical areas of the brain, including the hippocampus, which is important for relational memory and is reported to be sensitive to alcohol toxicity. However, the roles of DNA double-strand break (DSB) and its repair pathways, homologous recombination (HR), and non homologous end joining (NHEJ) in alcohol-induced hippocampal injury remain to be elucidated. The purpose of this first study was to assess alcohol-induced DNA DSB and the mechanism by which alcohol affects DSB repair pathways in rat hippocampus. Male Sprague Dawley rats (8-10 weeks old) were put on a 4-day binge ethanol treatment regimen. Control animals were maintained under similar conditions but were given the vehicle without ethanol. All animals were humanely euthanized 24 h after the last dose of ethanol administration and the hippocampi were dissected for immunoblot and immunohistochemistry analysis. Ethanol exposure caused increased 4-hydroxynonenal (4-HNE) staining as well as elevated gamma H2AX and 53BP1 foci in hippocampal cells. Immunoblot analysis showed decreased Mre11, Rad51, Rad50, and Ku86 as well as increased Bax and p21 in samples from ethanol-treated rats. Additionally, we also observed increased activated caspase3 staining in hippocampal cells 24 h after ethanol withdrawal. Taken together, our data demonstrated that ethanol concurrently induced DNA DSB, downregulated DSB repair pathway proteins, and increased apoptotic factors in hippocampal cells. We believe these findings will provide the impetus for further research on DNA DSB and its repair pathways in relation to alcohol toxicity in brain. (C) 2016 Elsevier Inc. All rights reserved.
机译：众所周知，狂犬病饮酒会导致大脑的临界区域损坏，包括海马，这对于关系记忆很重要，并且据报道对酒精毒性敏感。然而，DNA双链断裂（DSB）的作用及其修复途径，同源重组（HR）和非同源末端连接（NHEJ）仍然待阐明。第一次研究的目的是评估酒精诱导的DNA DNA DSB和酒精影响大鼠海马的DSB修复途径的机制。雄性Sprague Dawley大鼠（8-10周龄）被置于4天的狂欢乙醇治疗方案。在类似条件下保持对照动物，但没有乙醇给予载体。在最后剂量的乙醇给药后24小时，所有动物都在人道地安乐死，并且对海马进行免疫印迹和免疫组化分析。乙醇曝光引起的4-羟基（4-HNE）染色和海马细胞中γH2AX和53bp1焦点的升高。免疫斑分析显示来自乙醇处理大鼠的样品中的MRE11，RAD51，RAD50和Ku86以及增加的Bax和P21。另外，我们还观察到在乙醇戒断后24小时在海马细胞中染色增加了活性Caspase3。我们的数据一起展示了乙醇同时诱导DNA DMSB，下调的DSB修复途径蛋白，以及增加海马细胞中的凋亡因子。我们认为这些发现将为DNA DSB进行进一步研究的推动力，以及与脑中的酒精毒性相关的修复途径。 （c）2016年Elsevier Inc.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号