Relationship between lipopolysaccharide and reactive oxygen species in rat periodontitis model

点击翻译按钮获取中文摘要

Our previous study demonstrated that topical application of bacterial pathogens, i.e., lipopolysaccharide (LPS) and bacterial proteases, to gingival sulcus induced fatty liver. The purpose of this research project was to clarify the mechanism of fatty liver in rat periodontitis model, especially, to investigate the relationship between LPS and reactive oxygen species (ROS).In the year 2006, serum levels of LPS, ROS and tumor necrosis factor (TNF)-alpha were found to be elevated in rats with periodontitis compared to rats without periodontitis. Moreover, both concentrations of 8-hydroxydeoxyguanosine (8-OHdG) in liver homogenate and densities of 8-OHdG-positive liver cells were larger in the rats with periodontitis than in those without These results suggest that topically applied ITS affects liver directly, that cells in the periodontium respond LPS and produce ROS, that the ROS produced in periodontium affects liver directly, and that cytokines play some roles in the pathogenesis of fatty liver induced by periodontitis.In the year 2007, the effects of high cholesterol diet on the markers of oxidative stress in blood and liver of rats with periodontitis were investigated. Serum levels of reactive oxygen metabolites and hexanoyl-lysine and liver level of 8-OHdG were increased after feeding high cholesterol diet in the rats with periodontitis. These results suggest that high cholesterol diet has additive effects on periodontitis-induced oxidative damage in blood and liver.