RESUMO
Magnetic ß-cyclodextrin (ß-CD) porous polymer nanospheres (P-MCD) was fabricated by one-pot solvent thermal method using ß-CD immobilized Fe3O4 magnetic nanoparticles with tetrafluoroterephthalonitrile as the monomer. Compared with the ß-CD polymerization method reported in the literature,_ENREF_1 the synthetic route is effective and simple, thereby overcoming the harsh conditions that require nitrogen protection and always maintain anhydrous and oxygen-free. Moreover, the immobilization of ß-CD on magnetic nanoparticles is combined with the cross-linking polymerization of the cross-linker, leading to a good synergistic effect on the removal of contaminants. Meanwhile, the dispersibility of the magnetic carrier enhances the dispersion of the ß-CD porous polymer in the aqueous phase, and improves the inclusion adsorption performance and the adsorption process. P-MCD exhibited superior adsorption capacity and fast kinetics to MB. The maximum adsorption capacity of MB for P-MCD was 305.8â¯mgâ¯g -1, which is more than ß-CD modified Fe3O4 magnetic nanoparticles (Fe3O4@ß-CD). Moreover, the material had a short equilibrium time (5â¯min) for MB, high recovery and good recyclability (the adsorption efficiency was still above 86% after five repeated uses).
Assuntos
Magnetismo , Nanosferas , Poluentes Químicos da Água/química , Purificação da Água/métodos , beta-Ciclodextrinas/química , Adsorção , Cinética , Polímeros/química , PorosidadeRESUMO
BACKGROUND AND PURPOSE: Dysregulation of the miR-15a/16-1 cluster in plasma has been reported in patients with stroke as a potential biomarker for diagnostic and prognostic use. However, the essential role and therapeutic potential of the miR-15a/16-1 cluster in ischemic stroke are poorly understood. This study is aimed at investigating the regulatory role of the miR-15a/16-1 cluster in ischemic brain injury and insight mechanisms. METHODS: Adult male miR-15a/16-1 knockout and wild-type mice, or adult male C57 BL/6J mice injected via tail vein with the miR-15a/16-1-specific inhibitor (antagomir, 30 pmol/g), were subjected to 1 hour of middle cerebral artery occlusion and 72 hours of reperfusion. The neurological scores, brain infarct volume, brain water content, and neurobehavioral tests were then evaluated and analyzed. To explore underlying signaling pathways associated with alteration of miR-15a/16-1 activity, major proinflammatory cytokines were measured by quantitative polymerase chain reaction or ELISA and antiapoptotic proteins were examined by Western blotting. RESULTS: Genetic deletion of the miR-15a/16-1 cluster or intravenous delivery of miR-15a/16-1 antagomir significantly reduced cerebral infarct size, decreased brain water content, and improved neurological outcomes in stroke mice. Inhibition of miR-15a/16-1 significantly decreased the expression of the proinflammatory cytokines interleukin-6, monocyte chemoattractant protein-1, vascular cell adhesion molecule 1, tumor necrosis factor alpha, and increased Bcl-2 and Bcl-w levels in the ischemic brain regions. CONCLUSIONS: Our data indicate that pharmacological inhibition of the miR-15a/16-1 cluster reduces ischemic brain injury via both upregulation of antiapoptotic proteins and suppression of proinflammatory molecules. These results suggest that the miR-15a/16-1 cluster is a novel therapeutic target for ischemic stroke.