ABSTRACT
Objective@#To prepare a copper-nobium antibacterial coating on a titanium surface by a microarc oxidation-microwave hydrothermal two-step method and to study its surface structure and antibacterial properties.@*Methods@#Using titanium coated with a microarc oxidation coating (MAO group) as the substrate, copper and niobium were introduced by a microwave hydrothermal method in low (MHL-Cu group), medium (MHM-Cu group) and high (MHH-Cu group) copper chloride solutions and niobium oxalate (MH-Nb group) solutions, respectively. The component with the highest copper content was determined by energy spectrum analysis, and the copper-niobium composite coating (MH-Cu/Nb group) was prepared by microwave hydrothermal mixing with niobium oxalate. The microstructure, element distribution and phase composition of the specimens were characterized by scanning electron microscopy, energy dispersive spectrometry and X-ray diffraction, and the bacteriostatic effect of the coating onEscherichia coliand Staphylococcus aureus was determined by the film method. @* Results@#Energy dispersive spectrometry showed that Cu was introduced onto the surface of the MHL-Cu, MHM-Cu, and MHH-Cu groups, and the atomic ratios of copper in each group were （0.68 ± 0.04）%,（1.17 ± 0.06）%, and （1.64 ± 0.03）%. The difference between groups was statistically significant (P< 0.01). Scanning electron microscopy showed a crater-like porous structure on the surface of the MAO group, and the MHL-Cu, MHM-Cu, MHH-Cu, MH-Nb, MH-Cu/Nb groups maintained micropore morphology. The roughness increased with increasing Cu2+ concentration, in which the MH-Nb and MH-Cu/Nb groups showed gully like structures simultaneously. X-ray diffraction showed that the coating of the MAO group was mainly composed of titanium and anatase phase TiO2, and the coatings of the MHL-Cu, MHM-Cu, MHH-Cu, MH-Nb, MH-Cu/Nb groups were mainly composed of anatase and rutile phase TiO2. Compared with the MAO group, Escherichia coli and Staphylococcus aureus in the MHH-Cu, MH-Nb, MH-Cu/Nb groups decreased to varying degrees, with significant differences (P< 0.001); compared with the MH-Cu/Nb group, the colony number difference had statistical significance (P> 0.05)@*Conclusion@#The rough, porous coating containing copper and niobium prepared by the microarc oxidation-microwave hydrothermal two-step method can effectively inhibit the growth ofEscherichia coli and Staphylococcus aureus.
ABSTRACT
Propofol is an intravenous sedative hypnotic agent of which the growth-inhibitory effect has been reported on various cancers. However, the roles of propofol in endometrial cancer (EC) remain unclear. This study aimed to explore the effects of propofol on EC in vitro and in vivo. Different concentrations of propofol were used to treat Ishikawa cells. Colony number, cell viability, cell cycle, apoptosis, migration, and invasion were analyzed by colony formation, MTT, flow cytometry, and Transwell assays. In addition, the pcDNA3.1-Sox4 and Sox4 siRNA plasmids were transfected into Ishikawa cells to explore the relationship between propofol and Sox4 in EC cell proliferation. Tumor weight in vivo was measured by xenograft tumor model assay. Protein levels of cell cycle-related factors, apoptosis-related factors, matrix metalloproteinases 9 (MMP9), matrix metalloproteinases 2 (MMP2) and Wnt/β-catenin pathway were examined by western blot. Results showed that propofol significantly decreased colony numbers, inhibited cell viability, migration, and invasion but promoted apoptosis in a dose-dependent manner in Ishikawa cells. Moreover, propofol reduced the expression of Sox4 in a dose-dependent manner. Additionally, propofol significantly suppressed the proportions of Ki67+ cells, but Sox4 overexpression reversed the results. Furthermore, in vivo assay results showed that propofol inhibited tumor growth; however, the inhibitory effect was abolished by Sox4 overexpression. Moreover, propofol inhibited Sox4 expression via inactivation of Wnt/β-catenin signal pathway. Our study demonstrated that propofol inhibited cell proliferation, migration, and invasion but promoted apoptosis by regulation of Sox4 in EC cells. These findings might indicate a novel treatment strategy for EC.