急性移植物抗宿主病（aGVHD）是异基因造血干细胞移植后早期致死的重要并发症之一，预处理后肠黏膜屏障损伤、Th17/Treg细胞失衡是aGVHD发病的重要机制，而线粒体自噬失衡导致的氧自由基释放失控加剧肠黏膜屏障损伤、线粒体自噬PINK1/Parkin通路可以通过干预缺氧诱导因子调控Th17/Treg细胞比例。基于病机十九条，aGVHD胃肠道症状当属于“诸呕吐酸，暴注下迫，皆属于热”的范畴。本项目结合前期对线粒体的研究成果，建立半相合造血干细胞移植aGVHD小鼠模型，通过体内、体外实验两个方面，在组织、细胞、分子三个水平，深入探讨PINK1/Parkin通路在aGVHD发病中的作用，评价黄芩汤对aGVHD的体内外药效，明确其对该通路的调控作用，阐明其逆转肠黏膜屏障损伤、Th17/Treg细胞失衡从而打断aGVHD进程的具体机制。研究将为改善aGVHD症状提供新策略，提升移植后患者生存质量。

The damage of intestinal mucosa and imbalance of Th17 / Treg cells proportion after be treated with the chemotherapy regimen of the Allogeneic hematopoietic stem cell transplantation , are both the important mechanisms of acute graft versus host disease (aGVHD)as the crucial complication of Allo-HSCT.These years,there were some studies found that,oxygen free radical caused by mitochondrial autophagy imbalance can aggravate the damage of intensified intestinal mechanical barrier , and mitochondrial autophagy pathway can regulate the proportion of Th17 / Treg cells by intervening in hypoxia inducing factor.And based on article 19 pathogenesis, symptoms of aGVHD are belong to "All vomit acid, violent pouring, all belong to hot " .After we have some studies in mitochondria,this time we will establish the mouse model of aGVHD to prove the crucial rule of mitochondrial autophagy PINK1 / Parkin pathways in aGVHD,by using the in vivo and in vitro experiments,respectively.We will complish this subject in three level: tissue,cell and molecular level to. And then we will attempt to find whether huangqin soup can reduce ROS , to protect the intestinal mucosal barrier, reduce the release of inflammatory cytokines, and correction of Th17 /Treg cells imbalances,by regulating mitochondrial autophagy pathway,and eventually to interrupt the process of aGVHD.This research will offer new targets and methods for aGVHD treatment and promote the quality of life.