Design and In Vitro Activity of Furcellaran/Chitosan Multilayer Microcapsules for the Delivery of Glutathione and Empty Model Multilayer Microcapsules Based on Polysaccharides

In this study, multilayer microcapsules (two-layer and four-layer) based on furcellaran (FUR) and chitosan (CHIT) were produced, enclosing a tripeptide with an antioxidant effect-glutathione-in different concentrations. In addition, for the first time, an empty, four-layer microcapsule based on CHIT...

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Published in:Materials 2024-05, Vol.17 (9), p.2047
Main Authors: Drozdowska, Mariola, Piasna-Słupecka, Ewelina, Such, Aleksandra, Dziadek, Kinga, Krzyściak, Paweł, Kruk, Tomasz, Duraczyńska, Dorota, Morawska-Tota, Małgorzata, Jamróz, Ewelina
Format: Article
Language:English
Subjects:
Biopolymers
Cancer
Cell death
Chitosan
Chronic fatigue syndrome
Cytotoxicity
Emulsion polymerization
Glutathione
Ingredients
Multilayers
Polysaccharides
Thiols
Toxicity
Zeta potential
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Summary:In this study, multilayer microcapsules (two-layer and four-layer) based on furcellaran (FUR) and chitosan (CHIT) were produced, enclosing a tripeptide with an antioxidant effect-glutathione-in different concentrations. In addition, for the first time, an empty, four-layer microcapsule based on CHIT and FUR (ECAPS) was obtained, which can be used to contain sensitive, active substances of a hydrophobic nature. Layering was monitored using zeta potential, and the presence of the resulting capsules was confirmed by SEM imaging. In the current study, we also investigated whether the studied capsules had any effect on the Hep G2 cancer cell line. An attempt was also made to identify the possible molecular mechanism(s) by which the examined capsules suppressed the growth of Hep G2 cells. In this report, we demonstrate that the capsules suppressed the growth of cancer cells. This mechanism was linked to the modulation of the AKT/PI3K signaling pathway and the induction of the G2/M arrest cell cycle. Furthermore, the results indicate that the tested multilayer microcapsules induced cell death through an apoptotic pathway.
ISSN:1996-1944
1996-1944
DOI:10.3390/ma17092047