首页> 外文期刊>Life sciences >Molecular process in acute liver injury and regeneration induced by carbon tetrachloride.
【24h】

Molecular process in acute liver injury and regeneration induced by carbon tetrachloride.

机译:四氯化碳诱导急性肝损伤和再生的分子过程。

获取原文
获取原文并翻译 | 示例
           

摘要

Injection of carbon tetrachloride (CCl4) intraperitoneally into model animals induces acute liver injury mediated by reactive oxygen species (ROS) as normal metabolites in hepatocytes. In this study, the molecular process in this type of liver injury was analyzed from the aspect of liver function and regulatory factors. Down-regulation of liver-specific genes was accomplished through suppression of liver-enriched transcription factors and box A factors found in the catalase gene, and induction of NF-kappaB, AP-1 and a novel factor denoted as 'cx' in the catalase gene. Expression profiles of these genes were restored to normal levels in the late stage of injury (48 h). On the other hand, hepatocyte growth factor (HGF) and proliferating cell nuclear antigen (PCNA) were induced in the early stage (6 h) and 36 h, respectively. Interestingly, ERK2 was transiently activated at 3 h CCl4-treatment. These observations suggested that hepatotoxin by CCl4-injection concomitantly induces both processes in acute injury and liver regeneration.
机译:腹膜内注射四氯化碳(CCl4)到模型动物中,由肝细胞中的正常代谢产物-活性氧(ROS)介导急性肝损伤。在这项研究中,从肝功能和调节因子的角度分析了这种肝损伤的分子过程。肝脏特异性基因的下调是通过抑制过氧化氢酶基因中发现的富含肝脏的转录因子和box A因子,以及在过氧化氢酶中诱导NF-κB,AP-1和一个称为“ cx”的新因子来完成的。基因。这些基因的表达谱在损伤后期(48 h)恢复到正常水平。另一方面,肝细胞生长因子(HGF)和增殖细胞核抗原(PCNA)分别在早期(6 h)和36 h诱导。有趣的是,ERK2在3 h CCl4处理后被瞬时激活。这些观察结果表明,通过注射CCl4引起的肝毒素同时诱导急性损伤和肝再生过程。

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