一种针对受损线粒体的新型纳米颗粒系统，用于治疗帕金森病。
A novel nanoparticle system targeting damaged mitochondria for the treatment of Parkinson's disease.
机构信息
School of Life Science and Technology, Harbin Institute of Technology, Harbin 150080, People's Republic of China.
Department of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin 150080, China.
出版信息
Biomater Adv. 2022 Jul;138:212876. doi: 10.1016/j.bioadv.2022.212876. Epub 2022 May 23.
Mitochondrial damage is one of the primary causes of neuronal cell death in Parkinson's disease (PD). In PD patients, the mitochondrial damage can be repaired or irreversible. Therefore, mitochondrial damage repair becomes a promising strategy for PD treatment. In this research, hyaluronic acid nanoparticles (HA-NPs) of different molecular weights are used to protect the mitochondria and salvage the mild and limited damage in mitochondria. The HA-NPs with 2190 k Dalton (kDa) HA can improve the mitochondrial function of SH-SY5Y cells and PTEN induced putative kinase 1 (PINK1) knockout mouse embryo fibroblast (MEF) cells. In cases of irreversible damage, NPs with ubiquitin specific peptidase 30 (USP30) siRNA are used to promote mitophagy. Meanwhile, by adding PINK1 antibodies, the NPs can selectively target the irreversibly damaged mitochondria, preventing the excessive clearance of healthy mitochondria.
线粒体损伤是帕金森病（PD）中神经元细胞死亡的主要原因之一。在 PD 患者中，线粒体损伤可以被修复或不可逆转。因此，线粒体损伤修复成为 PD 治疗的一种有前途的策略。在这项研究中，使用不同分子量的透明质酸纳米粒子（HA-NPs）来保护线粒体并挽救线粒体的轻度和有限损伤。分子量为 2190kDa 的 HA-NPs 可以改善 SH-SY5Y 细胞和 PTEN 诱导的假定激酶 1（PINK1）敲除鼠胚胎成纤维细胞（MEF）细胞的线粒体功能。在不可逆损伤的情况下，使用带有泛素特异性肽酶 30（USP30）siRNA 的 NPs 来促进自噬。同时，通过添加 PINK1 抗体，这些 NPs 可以选择性地靶向不可逆损伤的线粒体，防止健康线粒体的过度清除。
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