期刊文献+

丹参素对缺血/再灌注损伤器官保护作用机制研究进展 被引量:4

A Comprehensive Review on Protective Mechanism of DanShenSu on Ischemia-reperfusion Injury in Multiple Organs
下载PDF
导出
摘要 缺血/再灌注损伤参与多种临床疾病的病理生理学过程,严重的缺血/再灌注损伤功能障碍是导致心肌梗死、脑卒中等致死的主要原因。丹参素是从中医临床最常用的活血化瘀类中药丹参(Radix Salviae Miltiorrhizae)中分离的活性成分,具有扩张冠状动脉、抑制血小板聚集、清除自由基、改善微循环、抗心肌损伤和抗炎等药理作用。随着对丹参素研究的不断深入,发现丹参素对心脏、肺、肾脏、胃肠道、脑和其他器官的缺血再灌注损伤具有保护作用,有望成为治疗缺血/再灌注损伤疾病的有效药物。本文就近年来丹参素对缺血/再灌注损伤器官的保护作用及潜在作用机制研究进展进行综述。 Ischemia/reperfusion injury is involved in the pathophysiological process of a variety of clinical diseases.Serious ischemia/reperfusion injury dysfunction is the main cause of myocardial infarction and stroke.DanShenSu is an active component isolated from Radix Salviaemiltiorrizae,which is the most commonly used Chinese medicine in the clinical practice of traditional Chinese medicine.It has the pharmacological effects of expanding coronary artery,inhibiting platelet aggregation,clearing free radicals,improving microcirculation,antagonizing myocardial injury and anti-inflammatory.With the development explore of DanShenSu research,DanShenSu has been found to have protective effects on the ischemia-reperfusion injury of heart,lung,kidney,gastrointestinal tract,brain and other organs,which is expected to be an effective drug for the treatment of ischemia-reperfusion injury.In this paper,we reviewed the recent research progress of DanShenSu on the protection and potential mechanism of ischemia/reperfusion injury organs.
作者 栗意 陈敏 王庭芳 张川 LI Yi;CHEN Min;WANG Ting-fang;ZHANG Chuan(Graduate School,Shanghai University of Traditional Chinese Medicine,Shanghai 201203,China;Department of Pharmacy,Shanghai University of Medicine&Health Sciences Affiliated Zhoupu Hospital,Shanghai 201318,China;School of Medicine,Shanghaiuniversity,Shanghai 200444,China)
出处 《海峡药学》 2020年第10期1-5,共5页 Strait Pharmaceutical Journal
基金 上海市卫计委青年科研项目,基于光亲和标记技术寻找Ⅰ类新药丹参素抗心肌缺血作用靶蛋白(20184Y0033)。
关键词 丹参素 缺血/再灌注损伤器官 作用机制 DanShenSu ischemia-reperfusion injury multiple organs mechanism of action
  • 相关文献

参考文献10

二级参考文献52

共引文献128

同被引文献87

引证文献4

二级引证文献23

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