Indirubin-3′-monoxime-loaded PLGA-PEG nanoparticles for potential Alzheimer's disease treatment

Medicine in Novel Technology and Devices

Zhenjiang Liang¹  Haiyan Li²  Xiaodong Cai³  Wei Cui³  Lingling Zhao⁴  Hui Tan⁵  Junying Liu⁵  Xiaopeng Ma⁵  Lingli Jin⁶  Hongze Liang⁶  Jiaying Zhang⁶  Mengxiang Yang⁷  Qiyao Wang⁷ 

[1] Corresponding author.;Corresponding authors.;Department of Endocrinology, The First Affiliated Hospital, Shenzhen University, Shenzhen, 518035, China;Department of Neurosurgery, The First Affiliated Hospital, Shenzhen University, Shenzhen, 518035, China;Department of Respiratory, Shenzhen Children's Hospital, Shenzhen, 518038, China;Faculty of Materials Science and Chemical Engineering, Ningbo University, Ningbo, 315211, China;Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China;

关键词: Nanoparticles;    Alzheimer's disease;    Drug delivery;    Indirubin-3′-monoxime;   

DOI  :  

来源: DOAJ

【 摘 要 】

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder, which is pathologically characterized by the deposits of β-amyloid (Aβ), and plays an important role in neuronal death. Indirubin-3′-monoxime (I3M) showed neuroprotective effects against Aβ-induced neuronal apoptosis. However, the use of I3M in AD treatment is limited due to its low bioavailability. Herein, PLGA-PEG nanoparticles were synthesized for I3M loading. I3M could release sustainedly sustain release from the I3M-loaded PLGA-PEG nanoparticles (PLGA-PEG-I3M NPs) without obvious burst release. What's more, the PLGA-PEG-I3M NPs could significantly promote the uptake of I3M by PC12 ​cells through nanoparticle-mediated transport, and improve the efficacy of I3M on the inhibition of Aβ fibrillization and oligomerization as well as the neuroprotective activity of I3M on Aβ oligomers-induced neuronal death. Thus, the PLGA-PEG-I3M NPs may be a promising platform for AD therapy.

【 授权许可】

Unknown