囊型包虫病是新疆等七省（区）高发的人畜共患病，占我国包虫病例的95%，其病原生物为细粒棘球蚴。据文献报道，青蒿素及其衍生物的过氧桥键经Fe2+催化产生超氧自由基，破坏DNA、蛋白等大分子物质，致使疟原虫等寄生虫死亡。我们实验发现青蒿素对细粒棘球蚴的活性、超微结构均有较大影响，及经其干预后虫体内超氧自由基含量和DNA损伤修复相关的基因表达量均增多，但其作用机制未知。因此，我们提出“青蒿素经超氧自由基致细粒棘球蚴DNA损伤，影响虫体活性”的科学假说，拟通过克隆细粒棘球蚴DNA损伤修复相关基因及鉴定功能，体外培养及体外动物模型，采用青蒿素及其衍生物、ROS清除剂及DNA损伤修复剂干预，应用透射电镜，DNA损伤检测，基因芯片，RNA干扰及RT-qPCR等技术，从形态，细胞，蛋白及基因表达等层面，验证假说。此研究将为阐明青蒿素及其衍生物抗囊型包虫病的作用机制和研发新型治疗包虫病药物奠定基础。

Cystic echinococcosis is the high incidence of zoonotic diseases in Xinjiang and other seven provinces (area). It is accounting for 95% of the hydatid cases which pathogens is Echinococcus granulosus. According to the published literature, the peroxide bridge of artemisinin and its its derivatives catalyzed by Fe2+ to generate superoxide free radical that damage DNA, protein and other macromolecules, resulting in the parasite death, such as Plasmodium. We found artemisinin had great effect on the vitality and ultrastructure of Echinococcus granulosus, and the superoxide free radical content and expression quantity of the gene related to DNA damage repair were increased. But its mechanism of action is unkonow. Therefor, we propose the scientific hypothesis that artemisinin damage the DNA of Echinococcus granulosus result in dead by superoxide free radical. This study will via in vivo and in vitro research, using transmission electron microscopy, DNA damage detection, gene chip, RNA interference, RT-qPCR and in situ hybridization, from the morphology, cell, protein and gene expression level, to test hypothesis. This study will lay the theoretical foundation for the elucidation of artemisinin and its derivatives against cystic hydatid disease mechanism and development of new drugs for the treatment of hydatid disease.