Impact Of Porphyromonas Gingivalis-Induced Ferroptosis On Vascular Endothelial Barrier.

This study aims to elucidate the effect of ferroptosis on the function of P.gingivalis-mediated periodontal endothelial barrier disruption. 1.C57BL/6J mice were randomly divided into control group, P.gingivalis group, and Fer-1+P.gingivalis group. Micro-CT was used to detect bone resorption and perform bone parameter analysis. FISH and immunofluorescence double staining were performed to examine the spatial distribution of P.gingivalis and marker CD31, and the expression of ferroptosis-related genes GPX4, SLC7A11, and TFR1. Related kits were used to measure serum concentrations of Inflammatory factors and serum iron. 2. An in vitro endothelial barrier model was constructed using HUVECs. TEER and FITC-Dextran were measured to verify endothelial barrier stability and permeability. WB, RT-qPCR, or related kits were employed to detect the expression levels of GPX4, SLC7A11, TFR1, PTGS2, MDA, ROS and pro-inflammatory factors in HUVECs. Inhibition of ferroptosis significantly down-regulated alveolar bone resorption induced by P.gingivalis, reduced P.gingivalis accumulation in brain tissue, and lowered serum levels of pro-inflammatory factors and related indicators. In P.gingivalis-stimulated HUVECs, the expression of ferroptosis-related protective genes GPX4 and SLC7A11 was significantly down-regulated, ROS and MDA levels were significantly increased, and endothelial barrier permeability was enhanced. Ferroptosis plays a major role in P.gingivalis compromises vascular endothelial barrier integrity, establishing a direct molecular link between periodontal infection and systemic endothelial dysfunction.