artykuł w czasopiśmie
Design and In Vitro Activity of Furcellaran/Chitosan Multilayer Microcapsules for the Delivery of Glutathione and Empty Model Multilayer Microcapsules Based on Polysaccharides
doi https://doi.org/10.3390/ma17092047
tytuł Design and In Vitro Activity of Furcellaran/Chitosan Multilayer Microcapsules for the Delivery of Glutathione and Empty Model Multilayer Microcapsules Based on Polysaccharides
autor Drozdowska ; Mariola
Piasna-Słupecka ; Ewelina
Such ; Aleksandra
Krzyściak ; Paweł
Kruk ; Tomasz
Duraczyńska ; Dorota
Dziadek ; Kinga
Morawska-Tota ; Małgorzata
Jamróz ; Ewelina
tytuł publikacji zbiorowej Materials
rok 2024
numer vol. 17, iss. 9
numer artykułu 2047
strony 1-17
ISSN/eISSN 1996-1944
pełny tekst https://www.mdpi.com/1996-1944/17/9/2047
licencja CC-BY
słowa kluczowe autorskie furcellaran/chitosan microcapsules
multilayer capsules
apoptosis
cytotoxicity
encapsulation
glutathione
abstrakt angielski 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. (original abstract)
finansowanie This work was supported by the National Center for Research and Development, Poland [Grant No.: LIDER/6/0016/L-11/19/NCBR/2020].
uwagi Summ. | Bibliogr.
język eng
Punkty ewaluacyjne 140.0000