ABSTRACT
This study examined the cell response to a TiO2 nanotubular surface (Ti-NT) for future biomedical applications. The level of cell attachment and spreading at 20 min and 60 min was evaluated by SEM. IL-6 and PGE2 secretion was evaluated by ELISA. In SEM analysis, the Ti-NT surface had more fully spread cells compared to the machined titanium surface (Ti-S). ELISA revealed that the level of IL-6 and PGE2 production was higher on the Ti-NT than on the Ti-S. These results suggest that a surface treatment with a nanotubular TiO2 surface enhances the early osteoblast responses, such as cell spreading and cytokine release, which are important for subsequent cell functions and bone healing in vivo.
Subject(s)
Nanotubes/chemistry , Skull/drug effects , Titanium/pharmacology , Animals , Cell Movement/drug effects , Cells, Cultured , Coated Materials, Biocompatible/chemistry , Dinoprostone/biosynthesis , Interleukin-6/biosynthesis , Metal Nanoparticles/chemistry , Metal Nanoparticles/ultrastructure , Microscopy, Electron, Scanning , Nanotechnology , Nanotubes/ultrastructure , Osteoclasts/cytology , Osteoclasts/drug effects , Osteoclasts/physiology , Rats , Skull/cytology , Skull/physiologyABSTRACT
The biological response of fetal rat calvarial cells on a TiO2 nanotubular surface (Ti-NT) was evaluated by cell viability assay, alkaline phosphatase (ALP) activity and reverse transcription polymerase chain reaction (RT-PCR) analysis. The cell viability assay showed no significant difference between the Ti-NT and smooth titanium surfaces (Ti-S). Ti-NT had better cellular responses with regard to the ALP activity and bone-associated markers, such as bone sialoprotein and osteocalcin mRNA than Ti-S. These results suggest that Ti-NT stimulate the differentiation into osteoblasts of fetal rat calvarial cells, potentially contributing to rapid osseointegration.
Subject(s)
Nanotubes/chemistry , Nanotubes/ultrastructure , Osteoblasts/cytology , Osteoblasts/physiology , Osteogenesis/physiology , Titanium/chemistry , Animals , Cell Adhesion , Cell Differentiation , Cells, Cultured , Macromolecular Substances/chemistry , Materials Testing , Molecular Conformation , Particle Size , Rats , Surface PropertiesABSTRACT
Ethanol induces hepatic steatosis via a complex mechanism that is not well understood. Among the variety of molecules that have been proposed to participate in this mechanism, the sterol regulatory element (SRE)-binding proteins (SREBPs) have been identified as attractive targets for therapeutic intervention. In the present study, we evaluated the effects of honokiol on alcoholic steatosis and investigated its possible effect on the inhibition of SREBP-1c maturation. In in vitro studies, H4IIEC3 rat hepatoma cells developed increased lipid droplets when exposed to ethanol, but co-treatment with honokiol reversed this effect. Honokiol inhibited the maturation of SREBP-1c and its translocation to the nucleus, the binding of nSREBP-1c to SRE or SRE-related sequences of its lipogenic target genes, and the expression of genes for fatty acid synthesis. In contrast, magnolol, a structural isomer of honokiol, had no effect on nSREBP-1c levels. Male Wistar rats fed with a standard Lieber-DeCarli ethanol diet for 4 weeks exhibited increased hepatic triglyceride and decreased hepatic glutathione levels, with concomitantly increased serum alanine aminotransferase and TNF-alpha levels. Daily administration of honokiol (10 mg/kg body weight) by gavage during the final 2 weeks of ethanol treatment completely reversed these effects on hepatotoxicity markers, including hepatic triglyceride, hepatic glutathione, and serum TNF-alpha, with efficacious abrogation of fat accumulation in the liver. Inhibition of SREBP-1c protein maturation and of the expression of Srebf1c and its target genes for hepatic lipogenesis were also observed in vivo. A chromatin immunoprecipitation assay demonstrated inhibition of specific binding of SREBP-1c to the Fas promoter by honokiol in vivo. These results demonstrate that honokiol has the potential to ameliorate alcoholic steatosis by blocking fatty acid synthesis regulated by SREBP-1c.
