Enhanced electrostatic interaction between chitosan-modified PLGA nanoparticle and tumor.
Int J Pharm
; 371(1-2): 142-7, 2009 Apr 17.
Article
en En
| MEDLINE
| ID: mdl-19118614
In our previous study, lung tumor-specific targeting of paclitaxel was achieved in mice by intravenous administration of chitosan-modified paclitaxel-loaded PLGA nanoparticles (C-NPs-paclitaxel). Transient formation of aggregates in the blood stream followed by enhanced trapping in the capillaries was proposed as a mechanism of the lung-specific accumulation of paclitaxel. In the present study, the mechanism of tumor lung preferential accumulation of paclitaxel from C-NPs-paclitaxel was investigated. Zeta potential and in vitro cellular cytotoxicity (A549 cells and CT-26 cells) of C-NPs-paclitaxel, and in vitro uptake of coumarin 6 to these cells from chitosan-modified coumarin 6 containing PLGA nanoparticles (C-NPs-coumarin 6) were examined as a function of pH (6.8, 7.4 and 8.0). The zeta potential of C-NPs-paclitaxel increased as the medium pH became more acidic. In vitro uptake of coumarin 6 by A549 cells and CT-26 cells was enhanced at lower pH for C-NPs-coumarin 6. In vitro cytotoxicity experiment with C-NPs-paclitaxel demonstrated enhanced cytotoxicity as the pH became more acidic. Therefore, enhanced electrostatic interaction between chitosan-modified PLGA nanoparticles and acidic microenvironment of tumor cells appears to be an underlying mechanism of lung tumor-specific accumulation of paclitaxel from C-NPs-paclitaxel.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Ácido Poliglicólico
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Portadores de Fármacos
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Paclitaxel
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Ácido Láctico
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Quitosano
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Nanopartículas
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Neoplasias Pulmonares
Límite:
Animals
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Humans
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Male
Idioma:
En
Revista:
Int J Pharm
Año:
2009
Tipo del documento:
Article
Pais de publicación:
Países Bajos