帕金森病（Parkinson's Disease, PD）是常见的神经退行性疾病之一。随着我国老龄化进程加速，其发病率逐年升高。因此，探寻PD新的有效治疗方案迫在眉睫。已有研究证实，DJ-1是较常见的与PD发病相关的基因，而且线粒体功能障碍在PD发病中起到重要的作用。大补阴丸是临床常用的治疗PD的经方，然而，大补阴丸治疗PD的具体分子机制（细胞信号转导机制）国内外文献尚未见报道。本研究小组经实验研究，大补阴丸在PD动物模型上验证了其具有线粒体保护效应。本项目在此基础上，从DJ-1基因过表达和靶向敲减正反两方面，深入探讨大补阴丸对线粒体功能保护效应的作用靶点，试图从PI3K/AKT信号途径揭示大补阴丸作用的分子机制，为PD临床治疗提供更为全面、详实的实验基础和理论依据。

Parkinson's disease (PD) is one of most common neurodegenerative diseases. With the accelerated aging process in China, its incidence is increasing year by year. Therefore, it's imminent to investigate new and effective treatment options in PD. Evidences have demonstrated that DJ-1 is one of common PD-related genes. Moreover, mitochondrial dysfunction has played an important role of in PD pathogenesis. Da-Bu-Yin-Wan (DBYW) is a classic formula that commonly used in PD clinical treatment. However, the literature has not yet reported the role of specific molecular mechanism (cell signal transduction mechanism) of DBYW. Our previous studies have shown that DBYW has mitochondrial protective effects in PD animal models. On this basis, using over expression and knock down of DJ-1 gene (both positive and negative aspects), this project aims to investigate the target role of DBYW on mitochondrial function protection, attempts to from the PI3K/AKT signaling pathway to reveals the molecular mechanism of DBYW, providing a more comprehensive, detailed experimental and theoretical basis for PD clinical treatment.