老年性聋病机错综复杂，前期动物研究初步表明, 国家专利方复方健耳剂具有阻止 ROS介导caspase启动耳蜗神经细胞凋亡的作用，但理论上调控ROS靶因子众多，具体调控机制及互相之间关系仍未明了，最新研究提示，该方在拮抗庆大霉素耳毒性动物模型中具有调控Trx-1和Trx-2作用，据此提出假说，Trx系统径路可能在老年性聋靶向调控ROS中扮演着重要角色，中药通过影响Trx系统及其外围各靶向调控蛋白质分子起到延缓老年性聋的关键作用，鉴此，我们将利用老年性聋动物模型，采用蛋白质组学、PCR、多重免疫荧光等分子生物学技术，配合耳蜗铺片、耳蜗切片等形态学研究方法，探索和明确Trx-ROS调控径路对老年性耳蜗神经细胞凋亡影响和这些靶向调控分子之间关系，进一步阐明老年性聋发病机制，揭示中药作用分子靶点与机制和中医治聋理论科学实质，为开发防聋治聋中药提供科学依据。

The pathogenesis of presbycusis is very complicated. Previous animal preliminary researchs showed that national patent prescription, healthy ear compound of traditional Chinese medicine(TCM), had the effect on preventing ROS-induced and caspase-mediated apoptosis of cochlear neurons. But theoretically, target factors of regulating ROS were numerous, and the concrete regulatory mechanisms and the relationship each other were still unknown. Latest research suggested that TCM possessed the effect on regulating Trx-1 and Trx-2 in animal models with antagonizing the ototoxicity of gentamicin, accordingly, put forward the hypothesis that pathway of Trx system may play an important role in regulating ROS by target proteins in presbycusis. The healthy ear compound plays a key role in delaying the apoptosis of cochlear neural cells by affecting the Trx system and its peripheral regulatory proteins. In view of this, we will use the animal model of presbycusis，apply proteomics, PCR，multi-overlap immunofluorescence and other molecular biological techniques, and be combined with the methods of morphological research such as cochlear slice and flat surface preparation, and then explore and confirm the influence of Trx-ROS regulating pathway on the apoptosis of cochlear neural cells with age-related hearing loss and the relationship each other in these targeting regulatory molecules so that could further clarify the pathogenesis of presbycusis , and reveal the molecular acting targets by using the TCM and scientific essence on theory of treating deafness by TCM, or provide scientific basis in order to exploit TCM for preventing and treating hearing loss.