自噬是依赖溶酶体降解多余或者受损的蛋白质和细胞器的过程。自噬缺陷在帕金森病（PD）发生发展中起关键作用。硫氧还蛋白（Trx）是重要的氧化还原调节蛋白，具有抵抗帕金森病的作用。然而，Trx是否可以改善PD中的自噬缺陷还未见报道。本项目将用mRFP-GFP-LC3腺病毒转染PC12细胞，高表达或低表达Trx，明确Trx对1-甲基-4-苯基-吡啶离子（MPP+）所致自噬流受损的调节作用；再用Trx高表达小鼠，以及中脑黑质区低表达小鼠（siRNA核团注射），确定Trx对1-甲基4-苯基-1,2,3,6四氢基吡啶（MPTP）所致LC3-II、p62、FOXO3A、DJ-1、LAMP-2A以及cathepsin D等表达的调节作用，弄清Trx调节PD中自噬缺陷的分子机制。该项目可以进一步阐明PD中自噬缺陷的分子机制，为PD的防治提供新视角。因此，该项目具有重要的学术研究价值和现实意义。

Autophagy refers to the progress by which superflous or damaged proteins and organelles are degraded by lysosomes. The defective autophagy plays a key role in pathogenesis of Parkinson Disease(PD). Thioredoxin (Trx) is an important redox protein and plays a role in resisting PD. However，whether Trx ameliorates defective autophagy in PD has not been reported. This project will confirm the role of Trx in regulating autophagic influx dysfuction induced by 1-methyl-4-phenylpyridiniumion (MPP+) by using mRFP-GFP-LC3 transfected PC12 together with Trx overexpression or siRNA. This study will determine the roles of Trx in regulating the expressions of LC3-II, p62, FOXO3A, DJ-1, LAMP-2A and cathepsin D induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by using Trx overexpression transgenic mice and low expression in substantia nigra pars compacta (siRNA injection in nuclei) and identify the molecular mechanism of Trx resisting defective autophagy in PD. This study will further clarify the mechanisms on defective autophagy in PD and provide new insight for preventing PD. Thus, this study has the important theory value and practical significance.