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

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。

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

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.