首页> 外文期刊>Hepato-gastroenterology. >Expression of matrix metalloproteinases in spontaneous regression of liver fibrosis.
【24h】

Expression of matrix metalloproteinases in spontaneous regression of liver fibrosis.

机译:基质金属蛋白酶在肝纤维化自发消退中的表达。

获取原文
获取原文并翻译 | 示例
           

摘要

BACKGROUND/AIMS: Spontaneous regression of liver fibrosis would depend on the degradation of the excessive matrix in the liver. In this study, we tried to determine the kinetics of the expression of genes for matrix metalloproteinase-2 and -13. METHODOLOGY: Liver fibrosis induced by carbon tetrachloride was resolved after withdrawal of this toxin. Histological staining for fibrous septa and determination of liver collagen content were used to evaluate the extent of liver fibrosis. Expression in liver of matrix metalloproteinase-2 and -13 was determined by reverse transcription-polymerase chain reaction. RESULTS: The fibrous septa became thinner and interrupted and liver fibrosis resolved rapidly within 10 days. Expression of matrix metalloproteinase-2 and -13 was elevated to 2.5- and 8.7-fold, respectively, at peak fibrosis. The former was maintained at 88%-76% and the later dropped rapidly to 30%-20% in the recovery periods. CONCLUSIONS: Resolution of liver fibrosis began within 10 days but only to 70%. Gene expression kinetics suggested metalloproteinase-13 might play a more important role in the resolution because it surged more markedly at peak fibrosis and returned to nearly basal levels in the recovery periods in parallel with liver collagen content.
机译:背景/目的:肝纤维化的自发消退将取决于肝脏中过量基质的降解。在这项研究中,我们试图确定基质金属蛋白酶2和-13基因表达的动力学。方法:撤消该毒素后,由四氯化碳引起的肝纤维化得以解决。纤维间隔的组织学染色和肝胶原含量的测定用于评估肝纤维化程度。通过逆转录-聚合酶链反应确定基质金属蛋白酶-2和-13在肝脏中的表达。结果:纤维间隔变薄并中断,肝纤维化在10天内迅速消退。在峰值纤维化时,基质金属蛋白酶2和-13的表达分别升高至2.5倍和8.7倍。在恢复期,前者保持在88%-76%,后者迅速下降到30%-20%。结论:肝纤维化的消退在10天内开始,但仅达到70%。基因表达动力学表明金属蛋白酶13可能在拆分中起更重要的作用,因为它在峰值纤维化时更明显地激增,并在恢复期间恢复到接近基础水平,与肝脏胶原蛋白含量平行。

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