tPA溶栓引起的出血性转化机制及小分子化合物干预作用研究进展  

Research progress on the mechanism of hemorrhagic transformation caused by tPA thrombolysis and the intervention effect of small molecule compounds

作　　者：黄娟 张米玲 余俊河 宫帅帅 寇俊萍[1] HUANG Juan;ZHANG Miling;YU Junhe;GONG Shuaishuai;KOU Junping(Department of Pharmacology of Chinese Materia Medica,School of Traditional Chinese Pharmacy,China Pharmaceutical University,Nanjing 211198,China)

机构地区：[1]中国药科大学中药学院中药药理与中医药系,江苏南京211198

出　　处：《药学研究》2024年第4期384-390,401,共8页Journal of Pharmaceutical Research

基　　金：江苏省自然科学基金(No.SBK20210432)。

摘　　要：组织型纤溶酶原激活剂(tissue type plasmin activator,tPA)是美国食品药品监督管理局唯一批准的用于急性缺血性卒中治疗的药物,但由于治疗时间窗狭窄以及会导致严重的出血性转化(hemorrhagic transformation,HT),其临床应用受到限制。本文拟从血脑屏障破坏、神经炎症、氧化应激以及亚硝酸应激等方面对HT发展的机制及近7年来发表在国内外期刊上的小分子化合物对HT保护的研究进展予以综述,为缺血性中风的新药开发和药物联用提供一定参考。Tissue type plasmin activator(tPA)is the only drug approved by the US Food and Drug Administration for the treatment of acute ischemic stroke.However,its clinical application is limited due to the narrow treatment time window and severe hemorrhagic transformation(HT).In this paper,the mechanism of HT development was reviewed from the perspectives of blood-brain barrier disruption,neuroinflammation,oxidative stress,and nitrite stress,as well as the research progress of small molecule compounds on HT protection published in domestic and foreign journals in the past seven years.This information would provide some clues and references for the new drug development and drug combination for the ischemic stroke.

关 键 词：组织型纤溶酶原激活剂 出血性转化 小分子化合物 研究进展 

分 类 号：R743.3[医药卫生—神经病学与精神病学]