dc.creator | Arancibia, Sergio | |
dc.creator | Barrientos, Andrea | |
dc.creator | Torrejón, Javiera | |
dc.creator | Escobar, Alejandro | |
dc.creator | Beltrán, Caroll J. | |
dc.date.accessioned | 2018-12-20T15:13:12Z | |
dc.date.available | 2018-12-20T15:13:12Z | |
dc.date.created | 2018-12-20T15:13:12Z | |
dc.date.issued | 2016 | |
dc.identifier | Nanomedicine, Volumen 11, Issue 10, 2018, Pages 1237-1251 | |
dc.identifier | 17486963 | |
dc.identifier | 17435889 | |
dc.identifier | 10.2217/nnm.16.39 | |
dc.identifier | https://repositorio.uchile.cl/handle/2250/158540 | |
dc.description.abstract | © 2015 Sergio Arancibia. Aim: In the present study, we examine the effects of copper oxide nanoparticles (CuNP) on macrophage immune response and the signaling pathways involved. Materials & Methods: A peritonitis model was used to determine in vivo immune cells recruitment, while primary macrophages were used as an in vitro model for the cellular and molecular analysis. Results: In vivo, CuNP induce significant macrophages recruitment to the site of injection. In vitro, in LPS-stimulated primary macrophages, the co-treatment with CuNP inhibited the production of NO in a dose-dependent manner. The mechanism underlying NO and proinflammatory cytokines inhibition was associated with an increased arginase activity. Macrophage stimulation with CuNP did not provoke any cytokine secretion; however, arginase inhibition promoted TNFα and MIP-1β production. In addition, CuNP induced the expression of COX-2 and the production of PGE2 through arginase activation. Conclusion: Our results demonstra | |
dc.language | en | |
dc.publisher | Future Medicine Ltd. | |
dc.rights | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | |
dc.rights | Attribution-NonCommercial-NoDerivs 3.0 Chile | |
dc.source | Nanomedicine | |
dc.subject | cyclooxygenase 2 | |
dc.subject | immunotoxicology | |
dc.subject | inducible nitric oxide synthase | |
dc.subject | nanomedicine | |
dc.title | Copper oxide nanoparticles recruit macrophages and modulate nitric oxide, proinflammatory cytokines and PGE2 production through arginase activation | |
dc.type | Artículos de revistas | |