학술논문
Bisdemethoxycurcumin (BDC)-Loaded H-Ferritin-Nanocages Mediate the Regulation of Inflammation in Alzheimer's Disease Patients.
Document Type
Article
Author
Gagliardi, Stella; Truffi, Marta; Tinelli, Veronica; Garofalo, Maria; Pandini, Cecilia; Cotta Ramusino, Matteo; Perini, Giulia; Costa, Alfredo; Negri, Sara; Mazzucchelli, Serena; Bonizzi, Arianna; Sitia, Leopoldo; Busacca, Maria; Sevieri, Marta; Mocchi, Michela; Ricciardi, Alessandra; Prosperi, Davide; Corsi, Fabio; Cereda, Cristina; Morasso, Carlo
Source
Subject
*ALZHEIMER'S patients
*BLOOD-brain barrier
*ALZHEIMER'S disease
*MACROPHAGE activation
*CEREBRAL cortex
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Language
ISSN
1661-6596
Abstract
Background: Bisdemethoxycurcumin (BDC) might be an inflammation inhibitor in Alzheimer's Disease (AD). However, BDC is almost insoluble in water, poorly absorbed by the organism, and degrades rapidly. We thus developed a new nanoformulation of BDC based on H-Ferritin nanocages (BDC-HFn). Methods: We tested the BDC-HFn solubility, stability, and ability to cross a blood–brain barrier (BBB) model. We tested the effect of BDC-HFn on AD and control (CTR) PBMCs to evaluate the transcriptomic profile by RNA-seq. Results: We developed a nanoformulation with a diameter of 12 nm to improve the solubility and stability. The comparison of the transcriptomics analyses between AD patients before and after BDC-HFn treatment showed a major number of DEG (2517). The pathway analysis showed that chemokines and macrophages activation differed between AD patients and controls after BDC-HFn treatment. BDC-HFn binds endothelial cells from the cerebral cortex and crosses through a BBB in vitro model. Conclusions: Our data showed how BDC-Hfn could improve the stability of BDC. Significant differences in genes associated with inflammation between the same patients before and after BDC-Hfn treatment have been found. Inflammatory genes that are upregulated between AD and CTR after BDC-HFn treatment are converted and downregulated, suggesting a possible therapeutic approach. [ABSTRACT FROM AUTHOR]