Controlled release of Clenbuterol from a hydroxyapatite carrier for the treatment of Alzheimer’s Disease

Alzheimer's disease is a neurodegenerative disorder, and A[beta] aggregation is considered to be the central process implicated in its pathogenesis. Current treatments are faced by challenges such as serious side effects and reduced drug bioavailability. In this study, we developed a drug deliv...

Full description

Saved in:
Bibliographic Details
Published in:Biomaterials research 2023, 27(00), , pp.2297-2315
Main Authors: Lin, Yi-Wen, Fang, Chih-Hsiang, Liang, Ya-Jyun, Yang, Ching-Yun, Kuo, Wei-Ting, Lin, Feng-Huei
Format: Article
Language:English
Subjects:
Alzheimer's disease
Amyloid beta
Bioavailability
Clenbuterol
Controlled release
Cytokines
Development and progression
Drug delivery
Drug delivery systems
Drug therapy
Drugs
Endosomes
Exocytosis
Fourier transforms
Hydrophobicity
Hydroxyapatite
Inflammation
Macrophages
Mediation
Morphology
Neurodegenerative diseases
Pathogenesis
Peptides
Product introduction
Saturated fatty acids
Stearic acid
Toxicity
Tumor necrosis factor-TNF
Vehicles
β-Amyloid
의공학
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Alzheimer's disease is a neurodegenerative disorder, and A[beta] aggregation is considered to be the central process implicated in its pathogenesis. Current treatments are faced by challenges such as serious side effects and reduced drug bioavailability. In this study, we developed a drug delivery system for intramuscular injection that uses cellular activity to achieve constant and long-term drug release. Synthesized mesoporous hydroxyapatite (SHAP) was prepared via co-precipitation, and hydrophobic surface modification using stearic acid was then used to load clenbuterol by physical absorption, thus creating the drug delivery system. Clenbuterol release was achieved through cellular activity, with macrophage uptake triggering lysosome/endosome disruption, cytoplasmic release, extracellular exocytosis, and subsequent systemic circulation. We found that clenbuterol-loaded SHAP enabled sustained release for more than 2 weeks and effectively modulated inflammation, reduced A[beta] oligomer-induced toxicity, and prevented A[beta] aggregation. Our findings suggest that treatment with clenbuterol loaded in this SHAP delivery system could be a promising strategy for treating Alzheimer's disease.
ISSN:2055-7124
1226-4601
2055-7124
DOI:10.1186/s40824-023-00432-4