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Relationship between lipopolysaccharide and reactive oxygen species in rat periodontitis model

大鼠牙周炎模型中脂多糖与活性氧的关系

基本信息

批准号：
18592277
负责人：
YAMAMOTO Tetsuo
金额：
$ 2.48万
依托单位：
Okayama University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18592277/
关键词：
periodontitis rat lipopolvsaccharide reactive oxygen species fatty liver oxidative stress cytokines high cholesterol diet 肝臓

项目摘要

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.

我们先前的研究表明，局部应用细菌病原体，即脂多糖(LPS)和细菌蛋白水解酶，可诱导牙龈沟诱发脂肪肝。本研究旨在阐明大鼠牙周炎模型中脂肪肝的发病机制，特别是探讨脂多糖与活性氧(ROS)的关系。2006年发现，与非牙周炎大鼠相比，牙周炎大鼠血清中的内毒素、ROS和肿瘤坏死因子-α水平明显升高。此外，有牙周炎的大鼠肝组织匀浆中8-羟基脱氧鸟苷(8-OHdG)浓度和8-OHdG阳性肝细胞密度均高于无牙周炎大鼠。提示局部应用8-OHdG直接影响肝脏，牙周组织细胞反应内毒素产生ROS，牙周组织产生的ROS直接影响肝脏，细胞因子在牙周炎诱导的脂肪肝发病机制中起一定作用。高脂饮食可使牙周炎大鼠血清活性氧代谢物和己酰赖氨酸水平升高，肝脏8-羟色胺水平升高。这些结果表明，高胆固醇饮食对牙周炎引起的血液和肝脏的氧化损伤具有相加的作用。