期刊文献+

肝肾纤维化动物模型的研究进展及评价 被引量:11

Research progress and evaluation of animal models of hepatorenal fibrosis
在线阅读 下载PDF
导出
摘要 肝、肾纤维化是由持续的肝、肾组织细胞损伤导致细胞外基质(extracellular matrix,ECM)过度沉积、实质细胞减少的病理过程,肝肾纤维化是慢性肝肾疾病持续进展的必经过程。除了器官移植,早期纤维化阶段现在被认为是治疗整个慢性疾病的关键阶段。目前有很多肝纤维化或肾纤维化的啮齿动物模型以及少量肝肾纤维化的复合模型可供疾病研究和药物筛选。本文对常用的肝、肾纤维化及其复合模型的造模方法与机制进行综述,并比较不同方法间的优势与不足,为日后不断建立和完善更加贴合临床的肝肾纤维化复合动物模型提供参考。 Fibrosis of the liver and kidneys is a pathological process in which extracellular matrix(ECM)is overdeposited and parenchyma cells are reduced by continuous damage to liver and kidney cells.Liver and kidney fibrosis is an inevitable process of chronic liver and kidney diseases.Except for organ transplantation,the early stage of fibrosis is now considered the key part of treatment for chronic disease.There are currently many rodent models of liver or kidney fibrosis,but only a few models with combined liver and renal fibrosis are available for research and drug screening.This paper summarizes the modeling method and mechanisms of common liver and kidney fibrosis,and composite models.We also compare the merits and demerits of different method to provide a reference for the future establishment and improvement of more clinically relevant compound animal models of liver and kidney fibrosis.
作者 庄子锐 王明亮 张婷 苏鹏亮 邵久针 印鑫 彭蕴茹 沈明勤 ZHUANG Zirui;WANG Mingliang;ZHANG Ting;SU Pengliang;SHAO Jiuzhen;YIN Xin;PENG Yunru;SHEN Mingqin(Jiangsu Province Academy of Traditional Chinese Medicine,Nanjing 210028,China;Affiliated Hospital of Integrated Traditional Chinese and Western Medicine,Nanjing University of Chinese Medicine,Nanjing 210028)
出处 《中国实验动物学报》 CAS CSCD 北大核心 2020年第6期845-852,共8页 Acta Laboratorium Animalis Scientia Sinica
基金 国家自然科学基金资助项目(81774178,81373888) 江苏省研究生实践创新计划资助项目(SJCX20_0572)。
关键词 肝纤维化 肾纤维化 肝肾纤维化复合模型 liver fibrosis kidney fibrosis liver and kidney fibrosis model
作者简介 庄子锐(1995-),女,在读研究生,研究方向:中药药理学研究。Email:542065186@qq.com;通信作者:彭蕴茹,女,研究员,硕士研究生导师,研究方向:中药药理学。Email:pengyunru@126.com;共同通信作者:沈明勤,研究员,硕士研究生导师,研究方向:中药药理学。Email:mqshen@163.com。
  • 相关文献

参考文献3

二级参考文献14

共引文献43

同被引文献113

引证文献11

二级引证文献45

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部