Data Sheet 1_Proteomics reveals periodontitis-driven oxidative stress and lipid metabolism disruption in NAFLD.csv

BackgroundPeriodontitis is increasingly recognized as a risk factor for non-alcoholic fatty liver disease (NAFLD), yet the underlying mechanisms remain unclear. Oxidative stress and lipid metabolism dysregulation may serve as key pathological links. This study investigates the impact of periodontitis on NAFLD progression and identifies molecular targets involved in hepatic oxidative stress and lipid alterations.
Materials and methodsA rat model of periodontitis was established via molar ligation. Hepatic pathology was assessed using histological staining, biochemical assays, and oxidative stress markers. Proteomic analysis identified differentially expressed proteins (DEPs) associated with lipid metabolism and inflammation. Functional enrichment analysis, protein-protein interaction (PPI) network construction, and hub proteins identification were conducted.
ResultsPeriodontitis significantly exacerbated hepatic lipid accumulation, fibrosis, and oxidative stress. Proteomic analysis identified 244 DEPs enriched in metabolic and inflammatory pathways. PPI network analysis revealed ACOX1, DBT, ACAA2, and HADHA as hub proteins. Downregulation of these proteins correlated with impaired lipid oxidation and hepatocellular injury in periodontitis-induced NAFLD.
ConclusionPeriodontitis accelerates NAFLD progression through oxidative stress and lipid metabolism dysfunction. ACOX1, DBT, ACAA2, and HADHA may serve as therapeutic targets. These findings highlight the importance of oral health in systemic metabolic disorders and suggest new intervention strategies.

背景：牙周炎（periodontitis）现已被越来越多地认为是非酒精性脂肪性肝病（non-alcoholic fatty liver disease, NAFLD）的危险因素，但其潜在发病机制仍未阐明。氧化应激与脂质代谢紊乱或为二者关联的关键病理通路。本研究旨在探讨牙周炎对NAFLD进展的影响，并筛选参与肝脏氧化应激及脂质代谢异常的分子靶点。
材料与方法：通过磨牙结扎法构建牙周炎大鼠模型。采用组织学染色、生化检测及氧化应激标志物评估肝脏病理状态。通过蛋白质组学分析筛选与脂质代谢及炎症相关的差异表达蛋白（differentially expressed proteins, DEPs），并开展功能富集分析、蛋白质相互作用（protein-protein interaction, PPI）网络构建及核心蛋白筛选。
结果：牙周炎可显著加重肝脏脂质蓄积、纤维化程度及氧化应激水平。蛋白质组学分析共筛选得到244个差异表达蛋白，这些蛋白显著富集于代谢及炎症通路。PPI网络分析显示ACOX1、DBT、ACAA2及HADHA为核心蛋白；上述蛋白的表达下调与牙周炎诱导的NAFLD中脂质氧化受损及肝细胞损伤密切相关。
结论：牙周炎可通过氧化应激与脂质代谢功能异常加速NAFLD进展，ACOX1、DBT、ACAA2及HADHA或可作为潜在治疗靶点。本研究结果凸显了口腔健康在全身代谢性疾病防治中的重要价值，并为相关干预策略提供了新的方向。