Drug-loading colloidal gels assembled from polymeric nanoparticles as an anti-inflammatory platform
Precise treatment of local inflammation is always challenging. Administration of anti-inflammatory drugs by direct injection has been considered as an efficient method for inflammation inhibition. In the present work, injectable drug-loading colloidal gels were developed with an aim to treat local i...
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Published in | New journal of chemistry Vol. 45; no. 31; pp. 13796 - 1385 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Cambridge
Royal Society of Chemistry
21.08.2021
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Subjects | |
Online Access | Get full text |
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Summary: | Precise treatment of local inflammation is always challenging. Administration of anti-inflammatory drugs by direct injection has been considered as an efficient method for inflammation inhibition. In the present work, injectable drug-loading colloidal gels were developed with an aim to treat local inflammation. Oppositely charged chitosan (CS) nanoparticles and aspirin-loading polylactic acid conjugated polyethylene glycol (PLA-PEG) nanoparticles were assembled into colloidal gels
via
electrostatic interaction among the nanoparticles. Such colloidal gels had stable three dimensional structure and shear-thinning rheological behavior. Under physiological conditions, the colloidal gels shed the nanoparticles autonomously in a sustained manner, which could reduce the loss of nanoparticles at the inflammation sites caused by permeation. The shed nanoparticles could be internalized by macrophages, as evidenced by fluorescence analysis. The PLA-PEG nanoparticles decomposed at intracellular pH and released the loaded aspirin. Both aspirin and CS nanoparticles inhibited the inflammation response of lipopolysaccharide (LPS)-stimulated macrophages, as suggested by the changes of typical inflammation factors and biomarkers. The colloidal gels represent a novel drug delivery platform for local inflammation therapy.
Injectable colloidal gels shed PLA-PEG and CS nanoparticles autonomously under physiological conditions and release aspirin to inhibit inflammation. |
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Bibliography: | 10.1039/d1nj02179f Electronic supplementary information (ESI) available. See DOI |
ISSN: | 1144-0546 1369-9261 |
DOI: | 10.1039/d1nj02179f |