RESUMEN
Oily particles pollution poses a tremendous threat to people's health, so it is urgent to develop air filtration materials with the ability of removing fine oily particles effectively. In this study, a nylon 6 multi-stage structured nanofiber membrane (PA6 MSNM) for effective air filtration of fine oily particles was designed and fabricated by adding a certain amount of tetrabutylammonium hexafluorophosphate (TBAHP) via one-step electrospinning. The PA6 MSNMs were composed of coarse trunk fibres and fine branching fibres. Benefiting from the properties of small pore size and high porosity, the resulting PA6 MSNMs exhibited high average filtration efficiency of 99.80% for oily aerosol particles of 0.20-4.59 µm, a low pressure drop of 251â Pa, and the high quality factor of 0.0248â Pa-1. More importantly, its filtration efficiencies for oily aerosol particles of 0.25 and 0.30 µm were up to 99.99% and 100.00%, respectively. It is expected that the multi-stage electrospun nanofiber membranes would have wide application prospects in air filtration, particularly for filtering oily particles.
RESUMEN
Objective: To determine the underlying mechanism of miR-34b/c in regulating doxorubicin (Dox)-induced myocardial cell injury.Methods: The viability of mouse myocardial cells HL-1 was detected by MTT assay. The apoptosis of HL-1 cells was detected by TUNEL assay. mRNA expressions of ITCH, TNF-α and IL-6 were measured by qRT-PCR. Protein levels of ITCH, NF-κB, TNF-α and IL-6 were measured by western blot. Dual luciferase assay was performed to detect the regulation of miR-34b/c on ITCH. Mouse model of cardiomyopathy was induced by intraperitoneal injection of Dox.Results: Dox reduced HL-1 cell viability and activated NF-κB pathway in HL-1 cells. miR-34b/c expressions were gradually up-regulated and ITCH expression was gradually down-regulated in Dox-treated HL-1 cells. miR-34b/c expression had negative correlation with the mRNA expression of ITCH. Besides, ITCH was a target of miR-34b/c. miR-34b/c mimic reduced cell viability, suppressed ITCH expression, increased TNF-α and IL-6 level, and promoted NF-κB expression in nucleus and cytoplasm of HL-1 cells. Whereas silencing miR-34 protected HL-1 cells through regulating ITCH. Finally, we demonstrated miR-34 antagomir-protected myocardial cells in mouse model of cardiomyopathy.Conclusion: miR-34b/c decreased HL-1 cell viability and promoted the secretion of proinflammatory cytokines in Dox-induced myocardial cells through ITCH/NF-κB pathway.