Bifunctional Fe3O4@Ag nanoparticles with both superparamagnetic and antibacterial properties were prepared by reducing silver nitrate on the surface of Fe3O4 nanoparticles using the water-in-oil microemulsion method. Formation of well-dispersed nanoparticles with sizes of 60 ± 20 nm was confirmed by transmission electron microscopy and dynamic light scattering. X-ray diffraction patterns and UV–visible spectroscopy indicated that both Fe3O4 and silver are present in the same particle. The superparamagnetism of Fe3O4@Ag nanoparticles was confirmed with a vibrating sample magnetometer. Their antibacterial activity was evaluated by means of minimum inhibitory concentration value, flow cytometry, and antibacterial rate assays. The results showed that Fe3O4@Ag nanoparticles presented good antibacterial performance against Escherichia coli (gram-negative bacteria), Staphylococcus epidermidis (gram-positive bacteria) and Bacillus subtilis (spore bacteria). Furthermore, Fe3O4@Ag nanoparticles can be easily removed from water by using a magnetic field to avoid contamination of surroundings. Reclaimed Fe3O4@Ag nanoparticles can still have antibacterial capability and can be reused.

Pulmonary fibrosis is the consequence of a variety of diseases with no satisfying treatment option. Therapy-induced fibrosis also limits the efficacy of chemotherapy and radiotherapy in numerous cancers. Here, we studied the potential of platelet-derived growth factor (PDGF) receptor tyrosine kinase inhibitors (RTKIs) to attenuate radiation-induced pulmonary fibrosis. Thoraces of C57BL/6 mice were irradiated (20 Gy), and mice were treated with three distinct PDGF RTKIs (SU9518, SU11657, or Imatinib). Irradiation was found to induce severe lung fibrosis resulting in dramatically reduced mouse survival. Treatment with PDGF RTKIs markedly attenuated the development of pulmonary fibrosis in excellent correlation with clinical, histological, and computed tomography results. Importantly, RTKIs also prolonged the life span of irradiated mice. We found that radiation up-regulated expression of PDGF (A–D) isoforms leading to phosphorylation of PDGF receptor, which was strongly inhibited by RTKIs. Our findings suggest a pivotal role of PDGF signaling in the pathogenesis of pulmonary fibrosis and indicate that inhibition of fibrogenesis, rather than inflammation, is critical to antifibrotic treatment. This study points the way to a potential new approach for treating idiopathic or therapy-related forms of lung fibrosis.

. TNF-␣ increases tyrosine phosphorylation of vascular endothelial cadherin and opens the paracellular pathway through fyn activation in human lung endothelia.